PENYAKIT KULIT VESIKOBULOSA

DAN
ERITROSKUAMOSA

Nur Hidayat
Bagian/SMF Ilmu Kesehatan Kulit dan Kelamin
Fakultas Kedokteran dan Ilmu Kesehatan
Universitas Tadulako/RSUD Undata
Palu
 PENYAKIT VESIKOBULOSA

DEFINISI PENYAKIT VESIKOBULOSA

Kelompok penyakit yang ditandai dengan gejala utama
erupsi vesikel dan bula.
Keterangan
Vesikel : penonjolan kulit dengan batas tegas, berisi cairan serous
dan diameternya < 1 cm, jika diameter > 1 cm disebut bula.

Vesikel Bula
 PATOFISIOLOGI TERJADINYA VESIKEL & BULA

Spongiosis:
Disebabkan karena masuknya cairan dan leukosit dari
dermis  edema interselular di antara sel-sel keratinosit
 ikatan antar sel melebar  ikatan putus. Contoh:
dermatitis kontak alergi (DKA)
PATOFISIOLOGI TERJADINYA VESIKEL & BULA

Degenerasi balon:
Disebabkan karena
infeksi intraseluler 
degenerasi balooning
 lisis sel  celah 
vesikel/bula.
Contoh: varicela,
herpes simpleks
 PATOFISIOLOGI TERJADINYA VESIKEL & BULA

Akantolisis:
Disebkan karena proses
akantolisis, yakni
hilangnya spina atau
akanta atau jembatan
antar sel, sehingga
terbentuk celah atau
rongga yang berisi
cairan.Biasanya
disebabkan autoimun.
Contoh : pemfigus
 PATOFISIOLOGI TERJADINYA VESIKEL & BULA

Sitolisis
Disebabkan kerusakan/ketidaksempurnaan komponen
sel/struktur lapisan kulit  sitolisis  sehingga terbentuk
celah. Contoh : epidermolisis bulosa
 MACAM PENYAKIT VESIKOBULOSA PADA

Diperantarai imunologi 1. Pemfigus vulgaris

2. Pemfigoid bulosa
3. Dermatitis herpetiformis
4. Linear IgA dermatoses
5. Herpes gestasiones
6. Cicatricial pemphigoid
7. Pemfigus paraneoplastik

Virus 1. Herpes simpleks

2. Varicella
3. Hand, foot & mouth disease
4. Herpangina
5. Campak
 MACAM PENYAKIT VESIKOBULOSA PADA

Herediter Epidermolisis bulosa

Lain-lain Eritema multiforme

Sindroma Stevens Johnson
Nekrolisis Epidermal Toksik
 PEMFIGUS VULGARIS

Gambaran klinis
• usia 50 - 60 th
• bula superfisial (supra basal),
dinding kendor (flacid), hipopion,
nikolsky sign + (bula cenderung
meluas bila kena tekanan), mudah
pecah  kulit terkelupas  krusta
• bau khas ~ tikus (mousy odor)
• Bula pada rongga mulut
mendahului (minggu – tahun)
sebelum pada kulit.
 Pemfigus vulgaris…

• predileksi: kulit kepala, wajah,

leher, lipatan aksila, inguinal,
periumbilikal, genital, mukosa :
bibir, buccal, palatum durum et
mole, lidah, mukosa alveolar &
ginggiva.

Nikolsky sign (+)

 Pemfigus vulgaris…

Patogenesis
Antibodi Ig G (+
komplemen) terhadap
desmoglein 3  akantolisis

Diagnosis banding:
• Pemfigoid bulosa
• Dermatits herpetiformis
• Stomatitis aphtosa
• Eritema multiforme
• Liken planus erosiva
• Pemfigoid membrana mukosa
 Pemfigus vulgaris…

Pemeriksaan:
• Pemeriksaan Tzanck : adanya sel akantolitik
• Patologi Anatomi : cleft suprabasal & akantolisis
• Direct immunofluorescence (DIF) : IgG dengan/tanpa
komplemen dg pola seperti jala (netlike pattern)
• Indirect immunofluorescence (IIF) : circulating IgG pada 90%
pasien

Terapi:
• Steroid sistemik (Prednison 2-3 mg/Kg BB)
• Imunosupresif (azatioprin, siklosporin, siklofosfamid,
mikofenolat mofetil)
• Plasmaferesis
• Imunoglobulin intravena
• Dll
 PEMFIGOID BULOSA

Gambaran klinis
• Usia 60 – 80 tahun
• Bula sub-epidermal, dinding tegang,
kadang hemoragis, kadang gatal
• Tanda Nikolsky (-)
• Predileksi : paha, aksila, lengan,
tungkai, perut, mukosa buccal
 PEMFIGOID BULOSA

Patogenesis
Antibodi IgG (+
komplemen) terhadap
BP antigen (BP 230/BP1
dan BP180/BP2)  bula
 Pemfigoid bulosa…

Diagnosis banding
•Dermatitis herpetiformis
•Pemfigus vulgaris

Pemeriksaan:
• Patologi Anatomi : cleft subepidermal dengan inflamasi
dermis atas, t.d limfosit, histiosit & eosinofil
• Direct immunofluorescence (DIF) : deposisi linear IgG dan
komplemen di dermo-epidermal juntion.
• Indirect immunofluorescence (IIF) : circulating IgG dengan
target komponen membran basal.
 Pemfigoid bulosa…

Terapi :
 Steroid sistemik (Prednison1 mg/Kg BB)
 Azatioprin, mikofenolat mofetil
 Dapson
 Tetrasiklin + nikotinamid
 Steroid topikal pada kasus ringan
 DERMATITIS HERPETIFORMIS

• Usia : 20 – 60 th.
• Papul eritem, plak
urtikaria, vesikel, bula,
berkelompok, simetris.
• Rasa gatal
• Predileksi :
ekstremitas ekstensor,
pantat, sakral,
skapula, wajah,
kepala.
• Berhubungan dengan
gluten sensitive
enteropathy.
 Dermatitis herpetiformis…

Patogenesis : antibodi (Ig

A) thdp antigen di usus 
kompleks Ag-Ab kmd
terdapat di kulit, ATAU Ig A
berikatan pd antigen di
kulit.Terjadi aktivasi
komplemen & penarikan
netrofil rusak jaringan.
Diferensial diagnosis :
• Dermatitis kontak alergika
• Papular urtikaria
• Pemfigoid bulosa
Terapi :
 Dapson 100-150 mg
 Sulfapiridin
 Gluten-free diet
 LINEAR Ig A DERMATOSES

• Papul, vesikel, bula,

berkelompok, simetris.
• Bula subepidermal.
• Rasa gatal.
• Predileksi : ekstremitas
ekstensor, pantat,
mukosa oral &
konjungtiva.
• Patogenesis : antibodi
(IgA) terhadap protein
97 Kda di membrana
basal.
 Linear IgA dermatoses…

• Diferensial diagnosis :
Dermatitis herpetiformis

• Terapi :
• Dapson
• Sulfapiridin
• Steroid dosis rendah
 HERPES SIMPLEKS

• Vesikel berkelompok dg dasar

eritem pada kulit/mukosa.
• Usia : kebanyakan dewasa, tp
anak s/d tua.
• Penyebab dan manifestasi :
HSV-1
Imunokompeten : primary
infection, primary herpetic primary herpetic gingivostomatitis
gingivostomatitis, herpes
labialis, herpetic whitlow,
aseptic meningitis, HSV
encephalitis
Imunokompromais :
widespread local infection,
chronic ulcers, disseminated
cutaneous & visceral infection.
 Herpes simpleks…

HSV-2 :
Imunokompeten : primary infection,
herpes genitalis, primer & rekuren,
herpetic whitlow, aseptic meningitis
Imunokompromais : widespread local
infection, chronic ulcer, disseminated
cutaneous & visceral infection

Patogenesis : virus  infeksi

kulit/mukosa tdk intak  replikasi
virus di parabasal sel epitelial  lisis
sel  vesikel (INFEKSI PRIMER) 
nervus sensori  ganglion
sensori/autonom (laten)  reaktivasi
virus  nervus sensori  vesikel
(INFEKSI SEKUNDER).
 Herpes simpleks…

Terapi :
Antiviral topikal (asiklovir, pensiklovir)
Antiviral oral (Infeksi primer : asiklovir 5 x 200 mg 7 hr,
valasiklovir 2 x 1 gr 7 hr. Infeksi rekuren : asiklovir 3 x
400 mg 5 hr, valasiklovir 2 x 500 mg 5 hr)
 VARICELLA

• Usia : kebanyakan anak-

anak
• Papul, vesikel, pustul, krusta
• Predileksi : wajah, badan,
ekstremitas, mukosa mulut,
hidung, konjungtiva, faring,
laring, trakea,
gastrointestinal, urinaria,
vagina.
• Penyebab : virus varicella-
zoster
 Varicela…

Terapi :
Antiviral (asiklovir 5 x 800 mg 5
hr, foscarnet 40 mg/KgBB iv.
 ERITEMA MULTIFORME

• Usia : 50% di bawah 20 th.

• Papul eritem iris-shape &
lesi vesikobula.
• Penyebab :
Obat (sulfonamid, fenitoin,
barbiturat, fenilbutazon,
penisilin, alopurinol)
Infeksi (herpes simpleks,
Mycoplasma)
Idiopatik
• Predileksi : ekstremitas
(telapak tangan & kaki) &
membrana mukosa (mulut,
konjungtiva)
 Eritema multiforme…

Diagnosis banding:
•Fixed Drug Eruption
•Primary herpetic ginggivosto-
matitis

Terapi :
Tergantung penyebab :
•HSV  antiviral
•Mycoplasma  antibiotik macrolid
•Topikal steroid
 SINDROMA STEVENS JOHNSON DAN
NEKROLISIS EPIDERMAL TOKSIK
• Usia : dewasa
• Epidermis nekrotik &
mengelupas, Nikolsky +.
• Predileksi :
• Wajah, badan, membrana
mukosa (bibir, buccal,
konjungtiva, genital, anal.
• Penyebab : obat (sulfa,
alopurinol, hidantoin,
karbamazepin, fenilbutazon,
piroksikam, penisilin,
sefalosporin, dll).
• TEN : ditambah bahan kimia,
Mycoplasma pneumonia, viral,
imunisasi
 SJS & TEN…

• Patogenesis : mekanisme
imunologis  reaksi sitotoksik
cell-mediated.
• Diagnosis banding:
• Eritema multiforme
• Sindroma syok toksik
• Graft-versus-host disease
• Terapi :
• Stop obat dicurigai
• Keseimbangan air & elektrolit.
• Kortikosteroid sistemik
• Terapi topikal spt luka bakar
• Antibiotika. Selesai
Selamat belajar
 Kelompok penyakit kulit dengan lesi utama
patch, plak atau papul eritematosa dengan
skuama

PSORIASIS
PITYRIASIS ROSEA
PITYRIASIS RUBRA PILARIS
LICHENOID ERUPTION
DERMATITIS EKSFOLIATIVA/ERYTHRODERMIA
etc
PAPULA: PENONJOLAN KULIT PADAT UKURAN<0,5 CM
SKUAMA: PENGELUPASAN KULIT BERLEBIHAN.
TAMPAK./ PATOLOGIS
 UNKNOWN CAUSE (MULTIFACTORIAL)
 CHRONIC AND RECIDIVE COURSE
 ERYTHROSQUAMOUS PLAQUE WITH
MICACEOUS MULTILAYERD SCALE

BASIC PATHOLOGY OF LESION

• CONTINOUS WOUND HEALING TYPE OF
KERATINOCYTE HYPER PROLIFERATION
•CONTINOUS INDUCTION BY INFLAMATORY CELL
• SHORTHERNING OF KERATINOCYTE TURN OVER
 PATHOGENESIS OF PSORIASIS

Triggering factors
 emotional stress
ENVIRONMENTAL FACTORS  season
PHYSICS,BIOLOGIC AND  trauma
EMOTIONAL
 drugs
 infection

PREPSORIATIC PSORIATIC SKIN

SKIN

genetic : IMUNOLOGIC AND

HLA DR. BW NON IMUNOLOGIK
PROCESSES
diet
race
 Schematic representation of generating psoriasis inflammatory
lesion from normal psoriatic skin. Starting from activation of native
APC’s to the maintenance of psoriatic lesion

Adapted from Prinz, 2003

 HISTOPATOLOGICAL FINDING

 DIFFUSE PARAKERATOSIS,
THINING OF SUPRA
PAPILARY EPIDERMIS,
 MICRO ABSES MUNRO,
 REGULER ACANTHOSIS,
 FINGER LIKE DERMAL
PAPILLAE
 EDEM OF DERMAL
PAPILLAE,
 SPARSE PERIVASCULAR
LYMPHO HISTIOCYTIC
INFILTRATRATION
PSORIASIS VULGARIS

COMMONEST FORM ,
SPECIFIC
ERYTHROSQUAMOUS
PLAQUE OVER
PROMINENCE AREA OF
THE SKIN
 Koebner phenomen ( isomorphic)
isomorphic eruption following
repetitive trauma ( LESIONS ARRANGED IN A LINE)

Wax drop phenomen

The micaceous scale be-
coming dull if scratched

Auspitz sign
pin point bleeding when pull off
the scale
 HISTOPATOLOGICAL FINDING

 DIFFUSE PARAKERATOSIS,
THINING OF SUPRA
PAPILARY EPIDERMIS,
 MICRO ABSES MUNRO,
 REGULER ACANTHOSIS,
 FINGER LIKE DERMAL
PAPILLAE
 EDEM OF DERMAL
PAPILLAE,
 SPARSE PERIVASCULAR
LYMPHO HISTIOCYTIC
INFILTRATRATION
 FLEXURAL / INVERSE PSORIASIS

SPECIFIC PLAQUE
AT FLEXURAL
AREA

SEBORIASIS -
PSORIASIS
SEBORHEIC
 GUTTATE PSORIASIS
ERUPTIVE
MULTIPLE, SMALL SIZE
DROP LIKE LESIONS
>> IN CHILDREN AS NEW
LESIONS
GENERALIZED PUSTULAR PSORIASIS (von
zumbusch)
generalized steril pustules, which are eruptive
accompanied high fever, WBC > 20.000/ML
DECREASE [Ca++] serum

PSORIASIS PUSTULAR
PALMOPLANTAR
Pustular Eruption limitted at
palmoplantar , recurrence
some time happen together with the
plaque type
PSORIASIS ARTHROPATHY

arthritis seronegative
•predilection: small joint
•persisten
•specific Radiologic pattern
Psoriasis of the nail

>>hand nails
 pitting nail
 yellowish
discoloration
 subungual
hyperkeratosis
 lateral onycholysis
BASIC MEDICAMENTATION
TOPICAL : TAR, SALICYLIC ACID, STEROID,TACROLYMUS
 SYSTEMIC : CYTOSTATIC AGENT (Cy-A, Mtx) , ISOTRETINOIN, “steroid”
COMBINATION : Irrad UV-B + tar ( Reg.Gaukerman)
irrad UV-A + psoralen (PUVA)

Drug considerance
 diseases severity ( PASI score )
 treatment history including medication side
effects
 patient situational status

Social/holistic approach
Sosialization of the illness to the patient and
family
 DERMATITIS EXFOLIATIVA (DE)
An eruptive skin disease as whole body erythema and
scaling.

Cause : several kinds of dermatosis (skin disease) which

undergone an eruptive state,ie:
1. Psoriasis/ other erythrosquamous eruption
2. Dermatitis ( Atopik, Seborrheic, Contact Allergic)
3. Drug eruption
4. Malignancy (cutaneous lymphoma)
5. Ichtyosis
8. Bullous disease (Pemphigus foliaceous)

Clinical sign and course

Generalized erythema and scaling
Lymphadenopathy, ectropion of the eyelid, edem at
lower extremities, some times fever, hypoproteiaemia,
leucocytosis, depletion [Ca]++ serum.
Psoriasis erythrodermia
• reactive psoriasis
•exfoliation > 75% body surface

BEFORE TREATMENT

8 WEEK AFTER TREATMENT

 PITYRIASIS ROSEA
E S E specific oval
erythematous patch,
multiple, fine scale ,
long axis in line with
Langer’s line,
spontaneous
regression
Etiology : unknown
(viral ?)
Herald patch, bigger
size surrounded by
the new lesions
(corymbi form pattern)
clinical course
start as single lesian
accompanied with
other sall lesions
generalized --- > faded Herald patch

Herald patch, close up

 Epidemiology: world wide, male/ female equal
child/ adult equal

Clinical manifestation:
Herald patch ----> smallest lesion surrounding
spread all-over body but face and palm/sole
Full blown on the back ---> tree form appearance
Lesions tend to distribute on clothed area.

Atypical forms : vesicular lesions

Self limitted in 6 - 12 weeks
cleared lesions left hypo - pigmented patch.

Therapy: symptomatic, anti inflammatory drugs ( steroid)

erythomycin systemic, UV-B photo therapy
PITYRIASIS RUBRA PILARIS

• RARE
• SPECIFIC :
ERYTHROSQUAMOUS
PAPULES, ACCUMINATE,
FOLLICULAR, TEND TO
COALESCE/
CONFLUENCY
• OLD LESION LEAVE
SMALL ISLANDS OF
HEALTHY SKIN
ETIOLOGY
• FAMMILIAL (Aut.Domin)
• VIT.A DEFFICIENCY ?
 LESION ON THE PALM AND SOLE

Yellowish colour
Keratotic sandal

Diffuse hyper keratosis on palms

The nail changes not specific

 PATHOGENESIS
INCREASE OF EPIDERMO-POIESIS UP TO 2-3 x NORMAL

CLINICAL MANIFESTATION
New Lesion : erythro squamous patches on the head (seborrhoiformis)
start with follicular erythematous papules.
Coalescence of lesions
In the palm and sole thick, luminence wax yellow colored
(keratodermic -sandal)
Old lesions : islands of normal skin between the plaque
Eruptive form: similar with dermatitis exfoliative of any cause

HISTOPATHOLOGY
• NOT DIAGNOSTIC BUT SPESIFIC
• HYPERKERATOSIS, PARAKERTOSIS ALTERNATING/FOLIKULER
• EUGRANULOSIS
TREATMENT
TOPICAL : STEROID
TAR + UV-B
SYSTEMIC: RETINOIC ACIOD
 LICHEN PLANUS
A COMMON CHRONIC INFLAMATORY SKIN DISEASE
WITH SPECIFIC CLINICAL AND HISTOPATHOLOGICAL
MANIFESTATION, UN KNOWN CAUSE

CLINICAL VARIATION
ERYTHRO SQUAMOUS, VESICO BULLOUS, HYPER-
TROPHIC,
ATROPHIK, ANULAR, FOLLICULAR, ACTINIC OR
ERYTHEMATOUS

ETIOPATHOGENESIS
INFECTION -PSYCHOGEN-GENETIC
ENZYMATIC IMMUNOLOGIC
CLINICAL MANIFESTATION
SINGLE LESION : FLAT TOPPED PAPULE,
POLYGONAL WITH WICKHAM STRIAE, DEEP
PURPLE HUE
DISCRETE
OLD LESION VARIED
MUCOSAL LESION :
WHITISH PLAQUE
(LACY WHITE APPEARANCE)
 Koebner sign

Flat topped polygonal lesion

with striae of Wickham