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PENYAKIT RADANG KULIT

NONINFEKSI DAN ALERGI


PSORIASIS
• Psoriasis may begin at any age, but it is uncommon under the age of 10 years.
• It is most likely to appear between the ages of 15 and 30 years.
• World-wide occurrence: Affects approximately 2 percent of Americans; prevalence
ranges from 0.1 percent to 3 percent in various populations.
• A chronic disorder with polygenic predisposition combined with triggering environmental
factors such as trauma, infection, or medication.
• Erythematous scaly papules and plaques; pustular and erythrodermic eruptions occur.
• Most common sites of involvement are scalp, elbows and knees, hands, feet, trunk, and
nails.
• Psoriatic arthritis occurs in 10 percent to 25 percent of patients; pustular and
erythrodermic forms may be associated with fever.
• Pathology is characterized by uniform elongation of the rete ridges, with dilated blood
vessels, thinning of the suprapapillary plate, and intermittent parakeratosis. Epidermal
and perivascular dermal infiltrates of lymphocytes, with neutrophils occasionally in
aggregates in the epidermis.
ETIOLOGY AND PATHOGENESIS
• Psoriasis is a chronic inflammatory skin disease, with a strong genetic basis,
characterized by complex alterations in epidermal growth and
differentiation and multiple biochemical, immunologic, and vascular
abnormalities, and a poorly understood relationship to nervous system
function.
• Historically, psoriasis was widely considered to be a primary disorder of
keratinocytes. With the discovery that the T-cell specific immunosuppressant
cyclosporin A (CsA) was highly active against psoriasis, most researchers
have focused on the immune system.
• Mekanisme peradangan kulit psoriasis cukup kompleks yang melibatkan
berbagai sitokin, kemokin, maupun faktor pertumbuhan yang
mengakibatkan gangguan regulasi keratinosit, sel-sel radang dan pembuluh
darah sehingga lesi tampak menebal dan berskuama tebal berlapis.
GEJALA KLINIS
• Keluhan berupa sedikit gatal dan panas di samping keluhan kosmetik
• Lesi pertama kali muncul pada tempat yang mudah terkena trauma antara
lain siku, lutut, sacrum, kepala dan genitalia, berupa macula eritema
berbatas tegas, tertutup skuama tebal trasnparan.
• Dapat menyerang kuku di maan permukaan kuku menjadi keruh,
kekuningan dan terdapat cekungan/pitting atau titik-titik pungtata,
menebal dan terdapat subungual hyperkeratosis sehingga kuku terangkat
dari dasarnya.
PEMERIKSAAN DAN DIAGNOSIS
• Karsvlek phenomena (fenomena bercak lilin) yaitu skuama psoriasis dikerok
akan terlihat warna keruh seperti kerokan lilin
• Austpitz sign, bila cara mengerok tadi dieruskan akan terlihat titik-titik
perdarahan oleh karena terkena papil dermis pada ujung-ujung yang
memanjang
• Koebner phenomena bila pada kulit yang masih normal terkena trauma
maka akan timbul lesi baru yang bersifat sama dengan yang telah ada.
TATALAKSANA
• Tergantung luas lesi kulit, lokasi lesi kulit dan umur penderita.
• Pengobatan kausal belum dapat diberikan sehingga pengobatan ditujukan
untuk:
• Menghilangkan faktor pencetus seperti stress diberi sedative, fokal infeksi dapat
berupa tonsillitis, gigi karies, investasi parasite.
• Menekan/menghilangkan lesi psoriasis yang telah ada meliputi:
• Pengobatan topical salep/krim yang mengandung steroid, tar (salep LCD 5%),
kalsipotriol atau tacrolimus.
• Pengobatan sistemik. Lesi luas: menggunakan methotrexate, pengobatan kombinasi
: PUVA, kombinasi topical dan sistemik.
PITIRASIS ROSEA
• Penyakit kulit rinfan dan dapt smebuh sendiri. Lesi berupa Makua, papula
eritematus berbentuk oval tertutup skuama tipis, sumbu panjang sejajar
pelipatan kulit.
• Predileks: bagian tubuh tertutup pakaian, leher-dagu.
• Gejala klinis:
• gejala konstitusi ±
• Gatal ringan-sedang/asimtomatik
• Herald patch/mother plaque, medalion sebagai lesi pertama
• makula bulat lonjong, tepi meninggi, lekat pada tepi.
• Sumbu panjang sejajar pelipatan kulit dan di punggung-gambaran pohon
cemara
• Tatalaksana:
• Antihistamin
• Bedak mengandung asidum salisikum
• Steroid topical/sistemuk, bila parah
• konseling
URTICARIA AND AGIOEDEMA
• Urticaria is defined as a skin lesion consisting of a wheal-and-flare reaction in
which localized intracutaneous edema (wheal) is surrounded by an area of
redness (erythema) that is typically pruritic.
• Individual hives can last from as briefly as 30 minutes to as long as 36 hours.
They can be as small as a millimeter or 6 to 8 inches in diameter (giant
urticaria). They blanch with pressure as the dilated blood vessels are
compressed, which also accounts for the central pallor of the wheal.
• The dilated blood vessels and increased permeability that characterize
urticaria are present in the superficial dermis and involve the venular plexus
in that location.
• Angioedema can be caused by the same pathogenic mechanisms as
urticaria, but the pathology is in the deep dermis and subcutaneous tissue
and swelling is the major manifestation. The overlying skin may be
erythematous or normal. There is less pruritus (fewer type C nerve endings at
the deeper cutaneous levels), but pain or burning may be present.
• Occurs acutely at some time in 20 percent of the population; incidence of chronic urticaria/angioedema is
approximately 0.5 percent.
• Acute urticaria/angioedema is caused by drugs, foods, occasionally infection in association with
immunoglobulin E-dependent mechanisms (allergy), or metabolic factors.
• Chronic urticaria/angioedema is an autoimmune disorder in 45 percent of patients.
• In the absence of urticaria, angioedema can be due to overproduction or impaired breakdown of bradykinin.
• Treatment of acute urticaria/angioedema relies on antihistamines and short courses of corticosteroids, and
identification and elimination of endogenous and exogenous causes.
• Treatment of C1 inhibitor deficiency includes androgenic agents, antifibrinolytic agents, and C1 inhibitor (C1
INH) concentrates. Fresh frozen plasma and C1 INH concentrate can abort acute episodes.
• Treatment of physical urticaria/angioedema includes high-dose antihistamine prophylaxis, except for delayed-
pressure urticaria.
• Treatment of chronic idiopathic or autoimmune urticaria/angioedema includes antihistamines (non-sedating
and sedating preparations), low-dose daily or alternate day corticosteroids, or cyclosporine.
FIXED DRUG ERUPTIONS

• FDEs usually appear as solitary, erythematous, bright red or dusky red


macules that may evolve into an edematous plaque; bullous-type lesions
may be present.
• FDEs are most commonly found on the genitalia and in the perianal area,
although they can occur anywhere on the skin surface.
• Some patients may complain of burning or stinging, and others may have
fever,
EPIDERMAL NECROLYSIS (SSJ-NET)
• Toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS) are acute life-threatening
mucocutaneous reactions characterized by extensive necrosis and detachment of the epidermis.
• Epidermal necrolysis (EN) is rare. The overall incidence of SJS and TEN was estimated at 1 to 6 cases
per million person-years and 0.4 to 1.2 cases per million person-years, respectively.
• Rare and life-threatening reaction, mainly drug-induced.
• Widespread apoptosis of keratinocytes provoked by the activation of a cell-mediated cytotoxic
reaction.
• Confluent purpuric and erythematous macules evolving to flaccid blisters and epidermal
detachment predominating on the trunk and upper limbs and associated with mucous membrane
involvement.
• Pathologic analysis shows full-thickness necrosis of epidermis associated with mild mononuclear cell
infiltrate.
• Early identification and withdrawal of suspect drugs are essential for good patient outcome.
• Treatment is mainly symptomatic.
• Pasien dikelompkkan dalam 3 kelompok berdasarkan luas area tubuh (body
surface area = BSA) yang mengalami pengelupasan (Nikolsky sign +) yaitu:
• SJS <10% BSA
• SJS/NET overlap : 10-30% BSA
• NET >30% BSA

1% BSA kurang lebih sama dengan luas permukaan 1 tangan


GAMBARAN KLINIS
• Gejala timbul dalam 8 minggu setelah awal pajanan obat
• Gejala non spesifik demam, sakit kepala, batuk/pilek, malaise selama 1-3
hari
• Lesi kulit: macula eritematosa atau purpuric, dijumpai esi target. Lesi kulit
meluas menjadi nekrotik sehingga terjadi bula kendur dengan tanda nikolsky
+. Lesi tersebar secara simetris pada wajah, badan, dan bagian proksimal
ekstremitas.
• Lesi mukosa: eritema dan erosi pada minimal 2 lokasi yaitu mulut dan
konjungtiva, dapat pula ditemukan erosi di area geniatlia.
• Keterlibatan organ dalam (paru, saluran cerna, ginjal) dapat terjadi namun
jarang.
TATALAKSANA
• Pertahankan keseimbangan cairan dan elektrolit
• Pemberian nutrisi
• Perawatan kulit secara aseptic
• Perawatan mata dan mukosa mulut
• Kortikosteroid sistemik
ERITRODERMA
• Kelainan pada kulit ditandai dengan adanya eritema universalins (90-100%),
biasanya disertai dengan skuama.
• Etiologi: alergi obat sistemik, perluasan penyakit kulit, penyakit sistemik
keganasan.
GAMBARAN KLINIS
• Eritroderma akibat alergi obat sistemik
• Riwayat konsumsi obat
• Waktu masuknya obat hingga timbul penyakit bervariasi segera sampai 2
minggu
• Terdapat eritema universal
• Skuama muncul pada stadium penyembuhan
• Eritroderma akibat perluasan penyakit kulit
• Eritroderma karena psoriasis: riwayat psoriasis sebelumnya, eritema tidak merata
pada tempat predileks psoriasis lesi lebih eritematosa dan agak meninggi
dibandingkan sekitarnya dan skuama di tempat itu lebih tebal.
• Terdapat pitting nail berupa lekukan miliar
• Eritroderma akibat penyakit sistemik termasuk keganasan
• Sindrom sezary
• Terjadi pada dewasa pria rata-rata berumur 64 tahun, wanita rata-rata 53 tahun
• Eritema warna merah mmembara yang universal, skuama dan sangat gatal
• Terdapat infiltrate kulit dan edema
• 1/3-1/2 pasien ditemukan splenomegaly, limfadenopati superfisial, alopesia,
hiperpigmentasi, hyperkeratosis palmaris dan plantaris dan kuku yang distrofik.
• Lab: leukositosis dan terdapat limfosit atipik (sel sezary)
• Disebut sindrom sezary bila ditemukan sel sezary yang beredar 1000/mm3 atau lebih
melebihi 10% sel yang beredar. Bila di bawah itu, disebut sindrom pre sezary.
TATALAKSANA
• Eritroderma karena obat: prednosin 4x10 mg
• Eritroderma karena perluasan penyakit kulit: prednisone 4x10-15 mg/hri.
• Sindrom sezary: prednisone 30 mg/hari
• Eritroderma kronis beri diet tinggi protein karena terlepasnya skuama
menyebabkan kehilangan protein.
DERMATITIS
INTRODUCTION DERMATITIS
• Dermatitis is a common skin disease
• Dermatitis or eczema
• Itis: inflammation
• dermatitis : non-infection skin inflammation with itch as main symptom,
recurrent-chronic
KNOWING DERMATITIS
• Look like simple
• The diagnosis should be established
• Example: dermatitis appearance equal to fungal infection but the treatment are
different. Glucocorticoid topical suppress skin immunity. Skin immunity are
important for infectious diseases
HOW TO DIAGNOSIS
•Repeated observation/bed-site
learning
•Careful examination:
•history
•dermatological
•diagnostic support: if it needed

Obtain t he diagnosis
PATHOGENESIS OF DERMATITIS
• Refers to an inflammatory response of the skin
• It may follow the stimulus (toxic, infectious, or alergic)
• The central role are T-cell lymphocyte:
• T-helper 1
• T-helper 2
• Releases mediators: cytokine, chemokine, growth factors
• Inflammation process: vasodilatation, edema and accumulations inflammatory cells
DERMATITIS
• an inflammation of
dermis and
epidermis (dermo-
epidermitis):
• Dilated vessels:
• blood cells
extravasations
• Edema, push the
keratinocytes to
cause cleft (blister)
EPIDERMAL THICKENING

• Epidermal thickening some degree:


• Increases skin marking, lichenification, fissures
PROGRESSION OF DERMATITIS
Acute

Subacute Chronic
DERMATITIS ACUTE-SUBACUTE

papules vesiclesl

plaques crusts
DERMATITIS CHRONIC

Lichenification and hyperpigmentation White scales/squamous


SIGN OF SUBACUTE
CLASSIC-DERMATITIS
• eritema
• squamation
• vesicles
• papules
• lichenification
• hiperpigmentation
DIFFERENTIAL DIAGNOSIS
DERMATITIS

Varicella Herpes zoster


DIFFERENTIAL DIAGNOSIS
DERMATITIS

dermatophytosis Urticaria
CLASSIFICATION OF DERMATITIS

Classification:
• Burton JL (etiological base)
• exogen
• endogen.
CLASSIFICATION OF DERMATITIS
Eczema exogen Eczema endogen
 Dermatitis contact iritan and alergic  Dermatitis atopic
 Dermatitis photocontact  Dermatitis seboroic
 Dermatitis numularis

 Dermatitis stasis
 Dermatitis hand n foot

 Dermatitis dry skin

J.L. Burton
TYPES OF DERMATITIS
• Atopic dermatitis
Chronic, relapsing skin inflammation, with dry
skin and pruritus.
• Allergic contact dermatitis
A delayed hypersensitivity reaction involving
allergens and antibodies.
• Irritant contact dermatitis
Exposure to irritating chemicals or
detergents.
TYPES OF DERMATITIS
• Stasis dermatitis
Occurs on the ankles and lower legs of people with venous insufficiency.
• Nummular dermatitis
Coin shaped patches that occur anywhere on the body in relation to dry
skin.
• Seborrheic dermatitis (cradle cap)
Yellow, greasy scales like dandruff on the scalp and hair-bearing areas of
the head, neck, upper chest, and flexural regions.
• Lichen simplex chronicus
A rash caused by long-term scratching of an area producing thickened skin.
ATOPIC DERMATITIS

• Intense pruritus and cutaneous


reactivity are cardinal features
• 3 phases of AD:
1. Infantile phase
2. Childhood phase
3. Adult phase
ATOPIC DERMATITIS

childhood

INFANTIL

ADULT
ALLERGIC VS IRRITANT CONTACT
DERMATITIS
ALLERGIC IRRITANT
Examples Nickel, fragrance, hair Water, soap
dye
Number of compounds Fewer Many
Distribution of reactions May spread beyond area Localized
Concentration of agent Can be very small High
needed to elicit reaction
Time course Sensitization in 2 weeks; Immediate to late
elicitation takes 24 – 72h
Immunology Delayed type Rupture of barrier skin
hypersensitivy reaction

Stewart, LA. Contact Dermatitis. In Fitzpatrick JE, Morelli JG editors: Dermatology Secrets in Color. 3rd
ed. Philadelphia, Pa: Elsevier; 2007. p. 77
CONTACT DERMATITIS
PHOTOCONTACT PHOTOTOXIC DERMATITIS
NUMMULAR DERMATITIS
• It has recently been considered a form of adult onset
atopic dermatitis.
• the characteristic round-to-oval erythematous plaques.
• commonly located on the extremities,

http://emedicine.medscape.com/article/1123605-overview
NUMULAR DERMATITIS
SEBHOROIC DERMATITIS
STASIS DERMATITIS
• Skin changes typical for patients with venous insufficiency,
include edema, varicosities, hyperpigmentation,
• Frequently involve the medial ankle, with symptoms
progressing to involve the foot and/or the calf.
• Erythematous, scaling, eczematous patches affecting the
lower extremity.
STASIS DERMATITIS
NEURODERMATITIS
• Chronic itching
• Initial lesion:
mechanic irritant
• Thickening of
epidermal and
upper dermis
• Symptoms in rest
Skin
lesion itch

scratch

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