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LCD Kuliah Dermatitis Wa2008

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1. Dermatitis Atopik 2. Dermatitis Kontak 3. Dermatitis Numularis 4. Dermatitis Seboroik 5. Dermatitis Statis 6. Eczema Infantum 7. Neurodermatitis ( Likhen Simpleks Kronikus) 8. Dermatitis Tangan & Kaki Dermatitis = Eczema made wardhana
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Page 1: LCD Kuliah Dermatitis Wa2008

1. Dermatitis Atopik2. Dermatitis Kontak3. Dermatitis Numularis4. Dermatitis Seboroik5. Dermatitis Statis6. Eczema Infantum7. Neurodermatitis ( Likhen Simpleks Kronikus)8. Dermatitis Tangan & Kaki

Dermatitis = Eczema

made wardhana

Page 2: LCD Kuliah Dermatitis Wa2008

Atopic dermatitis (AD) or atopic eczema is a• Chronically relapsing, pruritic, skin inflammation• Characterized primarily by an allergic diathesis • IgE mediated sensitization to environment allergen• Sometimes first appears in infancy. • Spesific clinical features: infant, child and adult

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Prevalence• Doubled or tripled in industrialized countries during the past

three decades;

• 15 to 30% of children and 2 to 10% of adults are affected.

• Atopic dermatitis frequently starts in early infancy (early-onset atopic dermatitis). in adults (late-onset atopic dermatitis).

• A total of 45% of all cases of atopic dermatitis begin within the first 6 months of life, 60% begin during the first year, and 85% begin before 5 years of age.

• Up to 70% of these children have a spontaneous remission before adolescence.

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Etiology• The etiology of AD has not been fully unknow• Hereditary/genetic and environmental factors

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• Hyperactive Th2 subset Thelper cells (associated with promotion of IgE production from B lymphocytes, differentiation of CD-4 T lymphocytes, suppression of Th1 cell activities, stimulation of proliferation, and differentiation of B lymphocytes)• Increased levels of serum IgE• Upregulation of IL-4• Increased eosinophils• Elevated levels of IgE activated mast cells• Disturbances in fatty acid metabolism/deficiencies of omega-6

fatty acids in plasma, adipose tissues, and formed blood elements

Pathophysiology - Immunopathogenesis

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Page 8: LCD Kuliah Dermatitis Wa2008
Page 9: LCD Kuliah Dermatitis Wa2008

Mediators of Mast Cells and Allergy

Mast CellMast CellBasophilBasophil

Blood VesselsBlood VesselsBlood VesselsBlood Vessels

Smooth MusclesSmooth MusclesSmooth MusclesSmooth Muscles

Mucus GlandsMucus GlandsMucus GlandsMucus Glands

Sensory NervesSensory NervesSensory NervesSensory Nerves

LeukocytesLeukocytesLeukocytesLeukocytes

H, PGDH, PGD22, , LTs, PAFLTs, PAF

bradykininbradykinin

HH

H, PGDH, PGD22, , LTs, PAFLTs, PAF

LTB4LTB4PAFPAFIL3, IL5IL3, IL5ChemokinesChemokines

Urticaria, AngioedemaUrticaria, AngioedemaLaryngeal edema, ShockLaryngeal edema, Shock

BronchospasmBronchospasmAbd. pain, VomitingAbd. pain, Vomiting

Diarrhea, RhinorheaDiarrhea, RhinorheaBronchial secretionBronchial secretion

ItchingItching

Inflammation - LPAR Inflammation - LPAR

AllergyChula

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The natural history of the illness may be described under thedifferent age groups:

1. Infancy (2 mo – 2 yr)Cheek & others, symetrical, erythem macule, papulo-vesicle

‘oozing’, moist crust

2. Childhood (> 2 y)antecubital and popliteal fossae, symetricalless exudattive, drier and more papular , Lichenified, slightly scaly

3. Adolescence and adulthood (> 12 y)localised erythematous macule or plaque, scaly, hyperkeratosis and lichenification

Clinical Feature

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Kriteria Diagnosis

Hanifin & LobitzHanifin & RajkaSvensonWilliam

Kriteria Hanifin & Rajka (modifikasi, 1990)

Major (basic) criteria - 3 or more of the following:1. pruritus2. typical morphology and distribution (flexural lichenification or linearity

in adults; facial and extensor involvement in infants and children)3. chronic or chronically-relapsing dermatitis4. Personal or family history of atopy (asthma, allergic rhinitis, atopic

dermatitis)

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Kriteria Minor ( 3 atau lebih)

1. Xerosis 2. Fisura periaurikuler3. Hiperlinearitas palmar 4. Keratosia pilaris5. Ig E meningkat 6. Dermatitis tangan7. Kheilitis 8. Dermatitis Scalp9. Mudah terjadi infeksi 10. Keratosis pilaris11. Pitiriasis alba 12. Dermatitis niple13. White dermographism 14. Katarak/keratokones15. Uji kulit positif 16. Garis Dennie-Morgan17. Kepucatan wajah 18. Awitan dini19. Faktor emosi 20. Tanda Hertog

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Treatment Guidelines for Atopic Dermatitis

• Moisturizers • For mild flare, mild (class VI or VII) corticosteroid to affected areas twice daily• For severe eczema, short term (no more than 2 wk) of medium- to high-potency topical

corticosteroids (class III through V) • Oral antibiotics for widespread, infected, flaring eczema• Topical antimicrobials, including mupirocin, bacitracin, 3% precipitated sulfur in petrolatum, 1% hydrocortisone, applied twice daily for infected eczema of the trunk and extremities• Antihistamines for pruritis• Eliminate precipitating environmental factors

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Page 15: LCD Kuliah Dermatitis Wa2008

Contact dermatitis refers to dermatitis caused by skin contact with an environmental agent. Contact dermatitis (CD) is an altered state of skin reactivity induced by exposure to an external agent. According to the mechanism of elicitation,

the following types of contact reactions may be distinguished:

1. allergic contact dermatitis (ACD),

2. irritant contact dermatitis (ICD),

3. phototoxic and photoallergic contact dermatitis,

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Chemicals or physical agents (primary irritants) damage the surface of the skin faster than the skin is able to repair the damage.

Well demarcated with a glazed surface but there may be redness, itching, swelling, blistering and scaling of the damaged area. • Amount and strength of the irritant • Length and frequency of exposure (eg. short heavy exposure

or repeated/prolonged low exposure) • Skin susceptibility (eg. thick, thin, oily, dry, very fair, previously damaged skin or pre-existing atopic tendency) • Environmental factors (eg. high or low temperature or humidity)

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Allergic contact dermatitisis (ACD) an immunologic inflammatory reaction of the skin due to

contact with an allergen. ACD is a cell mediated (delayed type) hypersensitivity reaction to environmental chemical or “sensitisers.” Different substances have different sensitizing potential, and there is individual susceptibility to sensitization by an allergen. The 2 distinct phases in a type IV hypersensitivity

reaction are the induction (ie, sensitization) phase and the elicitation phase.

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Treatment ACD

The only available etiologic treatment of ACD is elimination of the contact allergen. Systemic

AntihistamineCorticosteroid

TopicalAcute phase (papulo-vesiculo, oozing) wet bandage solutio NaCl 0,9 %Chronic phase topical steroid

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Dermatitis Numularis

Numuler, Eksim DiskoidPenyebab ???

Dermatitis atopikInfeksi :StafilokokusIritasi/kontaktanreaksi Id

Prevalensi : semua umur, semua jenisKlinis: gatal

polimorf akut, subakut, kronisnumuler : uang logan, soliter, mutipel

The term nummular means coin-shaped, so both terms describe the characteristic round (or oval) erythematous skin plaques.

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Neurodermatitis Sirkumskripta Likhen Simplek kronikus = Likhen Vidal

• orang dewasa• Penyebab ???• Faktor stres• Garukan yang berulang-ulang di suatu tempat

pergelangan, tangan, kuduk, betis

• Klinis : lesi kronis hiperkeratosis, likhenifikasi, hiperpigmentasi

• Terapi : cari penyebabnyaSteroid topikal kuat

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Stasis dermatitis is a rash of the lower legs which is due to poor return of blood to the heart. Usually the inner leg is more involved than the outer lower leg. Sometimes the rash breaks down into a sore resulting in a stasis ulcer. It affects people with varicose veins.

Stasis Dermatitis

Page 26: LCD Kuliah Dermatitis Wa2008

Stasis dermatitis is a rash of the lower legs which is due to poor return of blood to the heart.

Usually the inner leg is more involved than the outer lower leg. Sometimes the rash breaks down into a sore resulting in a stasis ulcer. It affects people with varicose veins.

Stasis Dermatitis

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Seborrheic Dermatitis Seborrheic dermatitis affects the scalp, central face,

and anterior chest.In adolescents and adults, it often presents as scalp

scaling (dandruff).

Seborrheic dermatitis also may cause mild to marked erythema of the nasolabial fold, often with scaling. Stress can cause flare-ups.

The scales are greasy, not dry, as commonly thought. An uncommon generalized form in infants may be linked to immunodeficiencies.

Topical therapy primarily consists of antifungal agents and low-potency steroids.

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• Gaangguan aliran darah vena daerah tungkai bawah(inkompeten katup vena)

• Tekanan vena meningkat ekstravasasi udem• lebih berat varises• faktor risiko : wanita gemuk, sering melahirkan,

pekerjaan berdiri, keturunan, ras• Prevalensi : >>> wanita setengah baya, gemuk• Klinis :

Lok : maleolus periferulkus kecil sukar sembuh/ kambuhantepi lesi hiperpigmentasi, variseslebih besar ulkus landai, pucat, melebar tak teratur

• Terapi : dermatitis secara umumuntuk varises : Sclerozing agent operasi

Page 29: LCD Kuliah Dermatitis Wa2008

Seborrheic eczema (also called seborrheic dermatitis, infantile seborrheic eczema, child/infantile eczema)

Most commonly associated with flaking and sometimes redness of the skin (www.medinfo.co.uk).

Occurs when there is inflammation of the skin where sebaceous glands are concentrated (Rouse).

Seborhheic or baby eczema is genetically determined, and therefore is not contagious. cradle cap

This type of eczema can affect the face, chest, eyebrows and eyelids, nose, ears, chin, forehead, and most commonly affects the scalp.

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Penyebab:Penyebab pasti ?????Peningkatan aktivitas kel.sebumHormonalInfeksi P. ovaleStafilokakusStres

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KlinisD Seboroika sicca – ketombe

Terutama kulit kepala -- skuama halus putih

D Seboroika oleosaWajah, sternum, interscapulaskuama tebal berminyak (warna kuning)Bayi baru lahir cradle cap : Leiner disease

PenatalaksanaanCari penyebabnyaAntihistaminTopikal krim hidrokortisonKulit kepala : sampo : selenium sulfida, ketokonazol

sulfurStres sedatif, penenang

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