Ciri Khas Histo PA 03/05/2017 22:29:00

 Dermatitis nummularis
- Akut: spongiosis, with/without spongiotic microvesicles
- Subakut plak: parakeratosis, scale-crust, epidermal hiperplasia, spongiosis of epidermis, mixed cell infiltrat in dermis
- Kronis: similar to LSK.
 LSK
- Hiperkeratosis, hipergranulosis, psoriasiform epidermal hiperplasia, penebalan papilary dermal collagen with coarse
collagen bundles and vertical streaks, infiltrat inflammatory bervariasi disekitar superf vascular plexus w/ limfosit,
histiosit dan eos
 Prurigo nodularis :
- Hiperkeratosis, hipergranulosis, psoriasiform epidermal hiperplasia (lbh kearah bulbous), penebalan papilary dermal
collagen dan kHAS: neural hipertrofi dgn thickened nerve bundles and in nerve fibers in S-100 stain
 Dishidrosis
- Akut: intraepidermal spongiotic vesicle, tidak melibatkan acrosyringia pada elektron mikrskop, bs tdp infiltrat
limfosit di epidermis, dgn infiltrat campuran pada dermis
- Kronis: hyperproliferation, hyperkeratotis epidermis or even psoriasiform epidermal hyperplasia
- PAS bs dipake u/ singkirkan elemen jamur
 TEN :
- Early stage: apoptotic KC in suprabasal layers  mjd full thickness necrosis and subepidermal detachment. Bs
melibatkan apoptosis sweat gland and HF. Moderately dense mononuclear cell infiltrate of papila dermis tu oleh
limfosit. Eos jarang
 EM :
- Eksositosis limfosit ke epidermis, satellite cell necrosis, spongiosis, degenerasi vakuolar pada sel membran basalis
dengan pembentukan celah sub epidermal. Demis edema dengan infiltrat sel mononuklear yang padat.
 AGEP :
- Spongiform subcorneal dan/ intraepidermal pustule, papilary dermis edema, perivascular infiltrat w/ netrofil dan
eksositosis of some eos.
 Drug induced BP :
- Perivaskular infiltrat of limfosit dan bbrp eos dan netrofil, intraepidermal vesikel dgn fokus KC nekrotik, thrombus in
dermal vessel, lack of tissue bound and circulating Antibasal membrane zone IgG
 Drug induced lichenoid eruptions:
- Focal parakeratosis, cytoid bodies in cornified and granular layers, adanya eos dan plasma cells in the inflamm
infiltrat, infiltrat around the deep vessels
 Pityriasis Alba:
- Markedly reduced pigmen in the epidermis, but no significant different in melanocyte count between lesi and normal
skin.
 Well’s Syndrome:
- Diffuse dermal infiltration w/ eos, histiosit dan foci of amorphous and/granular material associated w/ connective
tissue fibers, or flame figures
 Granuloma annulare:
- Lymphohistiocytic granuloma associated w/ varying degree of connective tissue degeneration and mucin deposition.
Inflammatory infiltrat berpola palisade/interstitial or mix.
- Typical: single/multiple foci of inflammation w/ central core of altered collagen (necrobiosis) surrounded by a wall of
palisaded histiocyte. Necrobiotic center biasanya oval, slightly basophilic, devoid of nuclei and marked by loss of
definition of collagen bundles & diminished/absent elastic tissue fibers.
- Stain for mucin and lipid (+)
 Erythema Nodosum :
- Septal panniculitis, widening of septa & early fibrosis, septal infiltrat of limf, histiosit, netrofil and eos. Infiltrat bs
masuk ke fat lobules disekitarnya, centrilobular necrosis of adipocyte is not seen
- Miescher’s granuloma: a discrete micronodular agregate of small histiocyte around a central stellate cleft

 Erythema induratum of Bazin / nodular vasculitis:
- Mostly lobular/mixed lobular and septal panniculitis w/ vasculitis
- Extensive necroses of adipocyte in the center of fat lobule
- Variable inflamm infiltrat in the fat lobule
- Vasculitis of the small veins and venules of fat lobule
 Lupus panniculitis:
- Vacuolar alteration of basal cell layer, thickened basement membr, mucin deposition between dermal collagen
bundles, superf and deep perivascular inflammatory infiltrat of lymph
- Basement membr thickening
 Lichen sclerosus:
- Atrophic epidermis, lichenoid infiltrat at DEJ, fibrosis with homogenization of acid mucopolysaccharides
 Morphea:
- Early: dense lymphocytic superficial and deep perivascular infiltrat with degeneration of collagen fibers
- Late: inflammation is replaced by dermal fibrosis
 Hailey-hailey : familial benign chronic pemphigus
- Partial loss of cohesion between suprabasal KC w/ an appearnace seperti dilapidated brick wall
 Acrokeratosis Verruciformis of Hopf
- Hiperkeratosis, hipergranulosis dan akantosis dgn papilomatosis, no acantholysis or dyskeratosis
- Spiky elevations: seperti church spires
 Darier Disease:
- Suprabasal cleft of epidermis containing acantholytic cells, rounded eosinofilic dyskeratotic cells in epidermis (Crops
ronds), hyperkeratosis, flattened parakeratotic cells in horny layer (grains)
 Grover Disease:
- Histo bervariasi, bisa seperti hailey hailey dgn detached keratinosit, focal spongiosis and epidermal hyperplasia
- Bisa pemphigus-like pattern with suprabasal acantholytic cleavage
 Incontinentia pigmenti:
- Areas of pigmentation: melanin laden melanophages, extensive deposits of melanin in basal cell layer and dermis,
vacuolisation and degeneration of basal cell layer
 HSP:
- Necrosis of blood vessels w/ deposition of fibrinoid material and dermal cellular infiltrat tdd netrofil w/ nuclear
debris, mononuclear cells and extravasated eritrosit.
- Deposit IgA1 in blood vessels, in skin , intestine and kidney
 Linear porokeratosis :
- Str corneum hiperkeratotik, cornoid lamela (+)., dibawahnya tdp hipogranulosis/ granular layer (-)
 Spitz nevus:
- Coalescent eosinofilic globules (Kamino bodies) (+) di intraepidermal, PAS (+)  bedanya ama melanoma:
melanoma globules lebih kecil lebih sulit ditemukan, single dan PAS negatif
- Epidermis hiperplastik, with elongated and bulbous pegs and knobs extending into dermis
 Keratoakantoma:
- Symmetric lesion w/ central keratotic core, tumor complex with large eosinofilix cells amixed w/ aytpical cells and
few mitoses, perineural growth of tumor cells (neurotropism)
- Epidermis tampak lipping or buttresing
 Bowen disease:
- Full thickness atipia of epitelium epidermal
 Trikoepitelioma:
- Infiltrasi sel basaloid monomorfik pada dermis bagian atas yang dikelilingi oleh stroma berbentuk fibrous dan
mengalami retraksi, agregasi sel germinativum monomorf pada dermis bagian atas
 Trichilemmal cyst or pilar cyst:
- Khas!! Tidak ada lapisan granular dalam dinding cyst,
- Isi kista keratin eosinofilik,
 Epidermoid cyst:
- Stratified squamous lining with intact granular layer!!!
 - Isi : central eosinofilic keratinaceous debris that can incite a foreign body reaction of multinucleated giant cells and
histiocyte when released into dermis and surrounding tissue
 Lupus eritematosus tumidus :
- Deposisi musin berlebihan, perivaskular superfisial dan inflamasi periadneksal
Diagnosis Histo PA Imunofluoresen
Pemfigus vulgaris Suprabasal bula dgn akantolisis pd granular layer, IgG di cell surface of KC in perilesi skin
tombstone appearance
Pemfigus foliaceous Akantolisis dibawah str corneum & lap granular, str IgG di cell surface of KC in perilesi skin
korneum srg hilang, subcorneal pustul dgn netrofil dan
akantolitik epidermal sel di dlm bula.
Pemfigus vegetans Suprabasilar acantholysis, papilomatosis of dermal papil,
hiperkeratosis, scale-crust formation
Ada intraepidermal abses tdd eos/neutrophil
Pemfigus eritematosus Sama seperti pemf vulgaris IgG dan C3 pada BMZ
Bullous pemfigoid Subepidermal blister w/ eosinofil, netrofil, limf, Linear IgG dan C3 di BMZ at the roof
monosit/macrofag in superf dermis side
Cicatrical pemphigoid Subepidermal blister, dermal leukosit infiltrat tdd limfosit Linear igG dan C3 di epitel basement
dan histiosit, plasma cells (+) in mucosa lesion, eos dan membran
netrofil (+) in skin lesions.
Linear IgA Subepidermal netrofil at basement membran, celah Linear IgA at dermal epidermal
subepidermal basement membrane.
Berhub dengan ulcerative collitis  sama2 butuh diet
gluten
Pemphigoid Subepidermal vesicle formation, dermal edema, infiltrat C3 with/without IgG dalam linear band
gestationes limfosit dan eos, t.u eos yang berjejer di DEJ, fokal basal di BMZ perilesi
necrosis. Ada bulbous, teardrop like vesicles. Eosinofil 
constant histologic feature of PG
EBA (autoimun thd Subepidermal bulla, fibrosis, milia formation, IgG di DEJ at dermal site (lower lamina
colagen 7) densa &/ sublamina densa)
DH Dermal papillary netrofil (microabses), subepidermal Granular IgA deposit di papila dermal,
vesiculation (separation of papillary tips from overlying bula terbentuk diatas lamina densa
epidermis) (didalam lamina lucida)
SCPD Kumpulan pustul kendur dlm pola anular/serpiginosa Deposit Ig A intraepidermal pada seluruh
Pustul subcorneal berisi PMN leukosit, pada epidermis lapisan epidermis atau terikat pada
terdapat slight edema n migrating leukocytes, ada bagian atasnya
perivaskular infiltrat pada dermis , no acantholytic cells, Terapi : dapson!!
 SCPD: berhubungan dengan : Pioderma gangrenosum, ulcerative colitis, Chron disease, non small cell lung cancer, apudoma,
rheumatoid arthritis, SLE, hipertiroidsm dan infeksi mycoplasma pneumoniae.
 Palmoplantar pustulosis :
o Kavitas intraepidermal dengan infiltrat leukosit PMN, beberapa infiltrat sel mast dan eosinofil
 Sweet syndrome
o Edema papila dermis dan infiltrat neutrofil matur yang tersebar pada dermis atas, illusion of vesiculation, without
leukocytoclastic vaskulitis
o UKK: gambaran relief of mountain range
 Juvenile xanthogranuloma
o Foam cells, foreign body giant cells, touton giant cells terutama pada dermis bagian atas
 Seboroik dermatitis pada HIV:
o Much more parakeratosis, nekrosis, limfosit dan fokal leukositosis
 Granuloma faciale :
o Gx: reddish brown papul dan plaq primarily involving the face
 o PA: kronik leukositoklastik vaskulitis dgn mixed infiltrat tdd eos, extensive perivaskular fibrin deposition dan dermal
fibrosis
 Tuberous sclerosis complex: (AD), mutasi pada TS1 or TSC2
o Collagen arranged in onionskin pattern around follicels and vessels
o Epidermis: hiperplasia melanocytic and flattening of rete ridges
 Bullous impetigo/ S4:
o bula di str granulosum, acantholysis (+)
 Liken nitidus:
o Central parakeratosis, epidermal thinning, loss of granular layer with focus of granuloma-appearing, inflammatory
cells and reactive, finger-like extensions of epidermis
 Miescher granuloma:
o Pada EN, suatu discrete micronodular aggregate of small histiocytes around a central stellate cleft.  khas early EN
o Bs ditemukan pada panniculitis lainnya
 Penyakit Aneh2 03/05/2017 22:29:00
o Well’s Syndrome :
 Single/multiple lesion mostly in extremities & trunk , may be painful/pruritic, bs jd bula, sering rekuren
 Bs resolve sendiri w/o scar within weeks-months
 Tx steroid systemic pd umumnya, tp bs jg pake minocycline, dapson, griseo and antihistamin. Mild case: topical steroid
is OK
 PA: flame figures (infiltrat difus di dermal dgn eosinofil, histiosit, dan amorf focus dan granula yg berhubungan dgn
serat jar ikat
o Kimura Disease & ALHE (angiolymphoid hyperplasia with eosinofilia ) or epitheloid hemangioma :
Kimura Disease ALHE
Race & age Mainly asian & younger age All race
Lesi Involve jar subQ, regional lymph nodes & Lesi lbh kecil, lebih superficial dan lebih banyak
salivary glands jumlahnya
Keluhan Asimtomatik Bs nyeri, gatal, atau pulsatil
Lab Periphearl blood eos (+) Periphearl blood eos (+)
Increased IgE level (+) -
Penyakit penyerta Renal disease -
Histo - Lymphoid prolif, often w/ germinal centers - Vascular prolif w/ numerous large epithelioid or
- fibrosis KHAS!! histiocytoid endothelial cells
- eosinophil abses may occur - fibrosis is limited/ -
- inconspicuous to numerous eos
Terapi : bisa surgery, systemic and intralesi steroid, inf-alpha tacrolimus
o Erosio interdigitalis blastomycetica: interdigital candidal /polymicrobial inf of hands/feet, usually kena ke interdigital space 3 &
4 underlying condition: moisture trapping
o Chronic mucocutaneous candidiasis:
 Inf candida pada skin, hair, nails and mucous membr.
 Berhubungan dgn endocrinopathy sprt hipoparatiroidism, hipoadrenalism, dan hipotiroidism, thymoma, immunodef.
 Cutaneous eruption: erythematous serpiginous border or areas of brownish desquamation on a background of mild
erythema
 Kuku: markedly thickened and dystrophic nail plates seluruh ketebalan kuku terkena candida, lipatan paronikia merah
dan edem, pus (+/-), fingertips sering bulbous
o Chromoblastomycosis:
 disbbkan oleh Phialophora verrucosa, Fonsecaea pedrosoi, Fonsecaea compactum, Wangiella dermatitidis,
Cladophialophora carrionii (dematiaceous fungi)
 UKK: solitary large verrucous plaque surrounded by a halo of erythema in calf
 Khas: tipikal sklerotik or muriform fungal cells, di kultur: black colonies with downy surface
 Tx: itra 200 mg/hari, terbi 250mg/hari bs kasih amphotericin B up to 1 mg/kg daily pada kasus yang luas , bedah
adjunctive tx
o Blastomycosis:
 Disebabkan oleh Blastomyces dermatitidis
 Lokasi utama: paru tp bs mengenai kulit, tulang, cns dan lainnya , krn kena debris kayu, daerah srg banjir, sungai dan
danau
 Pny cross reactivity dgn histoplasma
 Gx paru serupa dgn TBC , gx kulit: papul/ nodul yg ulserasi mengeluarkan pus, membesar membentuk lesi
hiperkeratotik dgn ulkus di bagian sentral / skar. Mirip pioderma gangrenosum
 KOH: tampak sel bulat sferis refraktil dengan broad based buds. Kultur: bentuk miselia pada suhu ruang, dan konidia
kecil bulat seperti buah pir
 Tx: itra 200-400 mg/hari  utk yang less severe/ localized. Voriconazole 6 bln. Amphotericin B (up to 1 mg/kg/hari) 
utk lesi widespread disseminated
o Sporotrikosis ;
 Oleh Sporothrix schenckii  kena dermis / subQ, ada 2 bentuk: subQ atau sistemik  jamur terdapat pada plant debris,
leaves, wood
 Bentuk limfangitik tangan kaki , dimulai dari nodul  pecah jd ulkus,  limfe menjadi bengkak  rantai nodul
lunak terbentuk sepanjang limfe
 Bentuk fixed: (jrg) infeksi tdpt pada 1 lokasi eg wajah terbentuk granuloma
 Sistemik bs meningitis, chronic lung nodules with cavitation, arthritis
 PA: small 3-5 yt surrounded by thick radiating eosinophilic fringe forming asteroid body! Netrofil microabsess
 Sporotrichin skin test
 Tx: itra 200 mg/hari, terbi 250 mg/hari continued for 1 week after clinical resolution
Bs tx topikal pake KI saturated 4-6 ml tid continued for 3-4 week after clinical cure
o Histoplasmosis
 Dimulai dgn infeksi paru2 sembuh sendiri,
  Acute progressive disseminated histoplasmosis: penyebaran luas ke organ lain sperti liver and spleen, RES, bone
marrow, ada weight loss and fever, srg pada pasien AIDS. UKK: papul, small nodul, or small molluscum like lesions
jd ulkus dangkal
 Chronic progressive disseminated histoplasmosis: oral/pharyngeal ulceration!!!, hepatosplenomegali, adrenal
insufisiensi. Ulkus mulut bs kena ke lidah dan buccal
 Kultur: koloni berwarna putih , dengan tuberculate macroconidia, microconidia (infeksius)
 Bisa periksa serologi dgn complement fixation titer indicate dissemination, deteksi precipitin pd imunodifusi, yg
mendeteksi adanya antibodi thd H dan M antigen
 PA: dermal macrophages berisi bentuk yeast dari Histoplasma capsulatum (bentul oval dan kecil 2-4 um )
o Mycetoma:
 Grains in center of abses, bs di foot, lower leg, hand,
 PA: chronic inflamm rx w/ netrophil abses and scattered giant cells and fibrosis
 Caused by eumycetoma dan actinomycetoma (Scedosporium apiospermum, dan actinomycetoma ec Nocardia sp,
Madurella mycetomatis, Streptomyces somaliensis )
 Black grain : fungi, red grain: actinomycete
 Tx: keto 200mg, itra 200mg, or voriconazole 200-400mg / hari selama bbrp bulan
o Penicilinosis
 Infeksi oleh P. Marneffei
 Bentuk yeast like cells yang terbagi oleh septa,  plg bagus terlihat dgn methenamine silver , bs dihighlight dgn
leishmanin
 Inhalasi melalui paru2, warna green grayish mold , ada diffusable red pigment
 UKK: papul umbilikasi yang membesar dan mengalami ulserasi, tersebar luas pada wajah dan trunkus, bs kena liver,
GIT, spleen, bone marrow
 DD: histoplasmosis, cryptococcosis
o Phaephymomycosis
 Caused by: Exophiala jeanselmei and W. dermatitidis
 UKK: formation of subcutaneous inflamm cysts or plaque, srg salah dgn synovial or Baker’s cyst, cystic lesion caused
by nonpigmented fungi (hyalohyphomycotic cysts), cyst wall tdd makrofag palisade, sel inflamatori, fungal hiphae
didalam macrophag zone
o Lobomycosis / keloidal blastomycosis
 Keloid like skin lesion on exposed site
 Cause by fungus Lacazia loboi , main tx: surgery
o SubQ mucormycosis (basidiobolomycosis)
 Caused by Basidiobolus ranarum (B. haptosporus) is more common in children
 2nd form: caused by Conidiobolus coronatus adult  kena daerah hidung inferior, meluas ke wajah
 gx: firm swelling (bengkak pelan2 membesar dan keras seperti kayu, tidak nyeri), woody cellulitis
 Splendore Hoeppli phenomenon: refraktil eosinophilic matterial in histo Pa,
 Tx: keto 400 mg/hari dan itra 100-200mg/hari
o Rhinosporidiosis:
 Caused by Rhinosporidium seeberi  development of polyps affecting mucous membrane studded with white flectks
o Erythema Dyschromicum Perstans
 Nama lain: ashy dermatosis, dermatosis cenicienta, erythema chronicum figuratum melanodermicum
 Khas: hyperpigmented macules & patches of variable shape and size, with ashen- gray to brown blue color
 Primarily on face, nectk trunk, proximal part of arm
 Slow progression without spontaneous regression
 PA: lichenoid dermatitis w/ vacuolisation of basal cell layer, occasional colloid bodies, increased epidermal melanin,
edema of papila dermis, mild limfohistiositik infiltrat, dermal melanophages
 No treatment
o Atrophoderma of Pasini-Pierini :
 Single/ multiple gray to violaceous brown atrophic patches from 1-10cm in diameter with sligh depression dgn khas
“Cliff drop” border
o Riehl Melanosis
 Female facial melanosis, mostly in middle aged women esp Mexican and Asian
 Rapid onset of reticular gray-brown to almost black hyperpigmentation, plg srg di face and neck
 PA: liquefactive degeneration of basal layer of epidermis, pigment incontinence in the dermis
 Repeated contact with sensitizer such as fragrance, pigments, optical whiteners
o Hailey-Hailey
 Dekade 2-4, di lokasi friction : neck, axilla, inframammary, groin, perineum, pain (+), itch(+), berbau!!
 UKK: crusted weeping erosions, vesicopustules, expanding annular plaque w/ peripheral scally border and vegetating
plaque w/ fissures (rhagades)
 Does not involve mukosa
 Longitudinal white lines on the fingernails!!
 Tx: 1st line: minimize friction and sweating, moderately potent/potent topical CS in comb with oral /topical AB &/
antifungal agents
 Prednisolone 20-30mg/dau
o Darier Disease : (AD)
 Discrete, greasy yellowish brown keratotic papules  predileksi daerah seboroik dan lipatan, bs fisura dan maserasi
 Bau badan! Fingernails dystrophics, red & white longitudinal bands
 Flat-topped papules, skin colored on dorsa of hands &/ feet: acrokeratosis verruciformis of Hopf
 Muncul pada usia 6-20 tahun , family history (+)
o Grover Disease :
 Nama lain: transient or persistent acantholytic dermatosis , male > 40 tahun, male: female: 3:1
 Triggered by sweating
 Ukk: itchy rash on sundamaged skin of trunk, itch may be intense, scattered pink or red brown papules w/
hiperkeratosis, pa;/]
 /;pm pulovesikel atau eczematous plak.
 Tx: topical steroid, emolien, retinoid, calcipotriol
o Rowell syndrome: varian dari cutaneous LE w/ erosive circinate lesions resembling EM
o Ectodermosis pluriorificialis (Fuchs syndrome): mucous membrane lesion without cutaneous involvement in EM (2-3 mucosal
site involved)
o Tinea nigra:
 Hortea werneckii,
 UKK: asimtomatic mottled brown to greenish black macule or patch with minimal to no scale, on palms or soles
 KOH: brown to olive colored thick branching hyphae along w/ oval to spindle shaped yeast yg muncul singly or in pairs
w/ central transverse septum
 Tx: keratolityc, whitfield’s oint, 2% SA, topical antifungal , dilanjutkan selama 2-4 minggu setelah sembuh
o Incontinentia pigmenti:
 Nama lain: Bloch – Sulzberger syndrome
 X-linked dominant, primarily in female, mutation in gene NEMO di kromosome X at Xq28
 Ada 4 tahap: 1) vesikular (dari lahir/segera setelah lahir), 2) verukosa (usia 2-8 minggu), 3) hiperpigmentasi (usia bbrp
bulan – dewasa), 4) hipopigmentasi (dari infancy sampe adulthood)  follows blaschko lines
 Ada kelainan ocular, dental, skeletal and CNS anomaly
 HistoPA: juml melanosit normal, epidermis lbh tipis, skin appendages ada yang hilang/berkurang
o Sclerema neonatorum :
 Tjd pada prematur newborn: diffuse hardening of the skin, tjd stelah 24 jam lahir, kulit keras, kaki dan imobile, looks
yellow and shiny
 Muncul pada usia 24 jam
 Yg berisiko tinggi : bayi dgn sepsis, hipoglikemi, asidosis metabolik, ato kelainan metabolik severe lainnya
 Biopsi : edema of fibrous septa surrounding fat lobules, no fat necrosis!!
 Subcutaneous fat necrosis of newborn; nodul merah keunguan batas tegas, keras, pada punggung, cheeks, pantat, tangan
paha
o Aplasia cutis congenita:
 Kulit gagal tumbuh seutuhnya, srg pada scalp,
 Ukk: sharply marginated atrophic macules on midline of posterior scalp, can be soliter or multiple, always hairless, may
appear vesicular, ulcerated or covered by thin epithelial membrane.
o Hair collar sign:
 ring of darker and/coarser terminal hairs on scalp, biasanya ditemukan surrounding ACC, dermoid cyst , encephalocele,
meningocele
 marker of cranial dysraphism
o Transient neonatal pustular melanosis :
 Idiopatik pustular eruption on newborn that heals with tiny brown-pigmented macules , munculnya superf vesikel dan
pustul, yg ruptur membentuk skuama kolaret
 Lokasi tersering : forehead and mandible area
o De Sanctis Cacchione syndrome :
 Cutaneous and ocular manif of classic Xeroderma pigmentosum + neurologic and somatic abN: microcephaly, mental
deterioration, low intteligence, hyporeflexia, choreoathetosis, ataxia, spasticity
o Porokeratosis:
 Classic: porokeratosis Mibelli : mulai saat anak2, asimtomatik small brown to skin colored annular papules, tepi annular,
hiperkeratotik setinggi 1 mm, khas! Longitudinal furrow!!! , bagian tengah lesi bs hiperpigmentasi/hipo, depressed,
atrofi/anhidrotic, berukuran bbrp mm-cm , biasanya unilateral
 Disseminated superf actinic porokeratosis: bentuk plg sering, small annular asimtomatik/mildly pruritic papuls berkisar
2-5 mm, tersebar simetris di ekstremitas, sun exposed sites
 Linear porokeratosis: bentuk jarang, muncul di awal anak2, bentuk tersering: lesi unilateral terbatas pada extremitas
mengikuti Blaschko lines, bentuk generalisata jg bs tp jarang, highest potensi for malignant degeneration
 Porokeratosis palmaris et plantaris disseminata : genodermatosis, AD inheritance, small uniform lesions that appear on
palms and soles, meluas ke bagian lain termasuk mukosa dan non sunexposed sites, lesi di tangan mjd hiperkeratotic,
longitudinal furrow lbh jelas , bilateral, simetris, lbh srg pd pria
 Punctate porokeratosis : pd ms remaja/dewasa, ukk: lesi hiperkeratotik kecil2 multipel yg tersebar, thin raised margin
pada palms and soles, muncul dgn pola linear / bergabung membentuk plak. PA: str corneum hiperkeratotik, cornoid
lamella menembus sel normal, sel keratin edema, spongiosis, nukleus mengecil, dibawah lapisan cornoid lamella lapisan
granuler berkurang  plg aman
  CDAGS syndrome: craniosynostosis, delayed closure of fontanel, anal anomalies, genitourinary malf, skin eruption 
atau disebut jg CAP syndrome (craniosynostosis, anal anomalis, porokeratosis): AR inheritane chromosome band
22q12-13  papul kecil menyebar nampak pada usia 1 bln pada wajah dan ekstremitas
 Tx: tidak perlu, 1st line: fotoproteksi, 5 FU, calcipotriol, imiquimod, topical steroid poten, keratolitik, topikal retinoid,
o Syarat2 elektrodesikasi dan kuretase pada tumor ganas BCC dan SCC:
 Tumor harus primer, distinct clinical border,
 Lokasi: pada daerah rekurensi rendah sperti trunkus, ekstremitas or non “H” zone of the face
 Have a superficial oe nodular histologic subtype,
 Ukuran < 1cm pada wajah dan < 2 cm pada badan dan ekstremitas
o PHACE syndrome:
 Posterior fossa brain malformations, Hemangioma (t.u facialis), Arterial anomalis, Cardiac anomalies and coarctation of
aorta, Eye abnormalities and Endocrine abnormalities
o Rombo syndrome:
 Multipel trikoepitelioma, atrophoderma, hipotrikosis, milia, BCC and peripheral vasodilation, teleangiektasis, acral
cyanosis
o Bazex-dupre-christol syndrome :
 Follicular atrophoderma (multiple ice pick marks or patulous follicles in dorsa of hands), milia, multiple BCC in
adolescent, hipotrikosis, localized hipohidrosis, pili torti
 X-link dominant, gene Xq24-q27
o Conradi-hunermann-happle syndrome (x-linked dominant chondrodysplasia punctata, CDPX2)
 X-linked dominant occurs only in girls, mutasi pada emopamil-binding protein gene at Xp11.23-p11.22
 UKK: ichthyosiform scaling erythroderma sepanjang garis Blaschko, resolves during 1 st year of life, replaced by bands
of follicular atrophoderma
 Ada hiperpigmentasi, katarak, scarring alopecia, saddle nose deformity, asymetric limb reduction defect, stippled
calcification of epiphysis
 PA: ichthyosis with keratotic follicular plug containing dystrophic calcification in newborns
o Nicolau Balus syndrome :
 Syringoma and milia
o Schimmelpenning syndrome: (linear nevus sebaceous syndrome )
 Linear nevus sebaceous, mental retardation, seizure, ophtalmic, skeletal, cardiovascular and urologic defect
o Waardenburg syndrome :
 Poliosis, defect pigmen iris, congenital deafness, developmental craniofacial abnormalitis
o Vogt-koyanagi-harada syndrome :
 Affect pigmented structures eg eye, inner ear, meninges and skin.  peran CD4 T Cells and Th1 cytokines
o Alezzandrini syndrome :
 Facial skin depigmentation, poliosis, deafness, unilateral tapetoretinal degeneration of eye
o Efek UV thd kulit:
 Immune system: menghambat activation effector T-cells, diminish cell mediated immune response,
 Mast cells: limit histmain release, UVA1: apoptosis mast cells
 Collagen: degradasi kolagen melalui peningkatan produksi IL1 & IL-6, yang mengaktivasi MMP1
 Keratinosit epidermis: akantosis, penebalan str corneum
 Melanosit: stimulate melanogenesis
o Fitz Hugh Curtis Syndrome : infkesi GO or CT dengan inflamasi pada liver capsule, berhub dgn infeksi genitourinary, ada pada
¼ wanita dengan PID  Gx: right upper quadrant pain and tenderness w/ abN liver fx test
o Diaper Rash Dermatitis:
 Granuloma Gluteale Infantum: nodul merah keunguan ukuran berbeda pada anak 2-9 bulan
 Infantile Granular Parakeratosis: bilateral linear plaq in the inguinal folds and eritemathous geometric plaq underlying
pressure point
 Jacquet Erosive Dermatitis: ulkus punch out batas tegas, erosi dengan tepi meninggi
 Pseudoverucous papules and nodules :
 Miliaria rubra: biasa pada komponen plastik dari pampers
 Candida : bright red eritem moist papul, patch plak, ada lesi satelit!!
 Irritant diaper dermatitis: eritem moist patch dengan skuama tipis
o LGV: saxophone penis, esthiomene, limforroid, frozen pelvis , genital elephantiasis w/ ulcer and fistula : tertiary stage!!
o Liken planus
 Khas: papul bentuk simetris, berkelompok, eritem to keunguan , flat topped, poligonal , surface is shiny and ada white
lines (Wickham Striae)
 Predileksi tersebar luas t.u pada flexural arms and leg
 PA: basal epidermal KC damage and lichenoid interface lymphocytic reaction, likenoid interface reaction, sawtooth!!
Ada Civatte bodies pada DEJ (colloid hyaline borders)!!
 Graham little syndrome: follikular lichen planus of skin &/or scalp, multifocal cicatricial alopecia of scalp, nonscarring
alopecia of axila and pubic areas
 Hipertropik liken planus: pada ekstremitas, bentuk PALING GATAL!!, lesi menebal dan meninggi membentuk
follicular induration and chlak like scale. Sembuh dgn skar dan hipo/hiperpigmentasi, biasanya ada insuf vena kronis
  Atropik liken planus: jarang, papul ato plak putih kebiruan batas tegas, dengan atrofi superf pada bag tengah. Plg sering
pada ekstremitas bawah/trunkus
 Vesikobulous liken planus: jarang, bula muncul pada extremitas, pada oral: painful erosion. PA: subepidermal
separation!
 Erosive ulcerative liken planus: erosi, ulkus dan jar granulasi dan skar pada toes, sela jari interdigital, soles.

o Congenital diffuse Hipermelanosis :

 Linear type :
o Linear and Whorled Nevoid hipermelanosis
o Incontinentia pigmenti
 Reticular type :
o Diskeratosis congenita
o Congenital circumscirbed hipermelanosis :
Dengan dermal melanosis Dengan lentiginosis Dengan café au lait macules
Nevus ota Familial lentiginosis syndrome NF-1
Nevus ito Peutz Jeghers syndrome  plg srg dgn Mccune Albright syndrome
keganasan GIT
Mongolian spot LEOPARD syndrome
Dermal melanocyte harmatoma
 Acquired circumscribed hypermelanosis:
 Phytophotodermatitis
 Flagellate pigmentation due to bleomycin
 Flagellate mushroom dermatitis
 nevus of hori ,
 Becker nevus
 Ephelids
 PIH
 Familial periorbital hiperpigmentation
 Partial unilateral lentiginosis
 Riehl melanosis
 Cutaneous amyloidosis
 Atrophoderma of pasini pierini
 FDE
 Eritema diskromium perstans
o Acquired diffuse patterned or reticular :
 Erythema ab igne : chronic exposure to moderate heat
 Prurigo pigmentosa
o Blueberry Muffin baby:
 Congenital human CMV:violaceous papule and macules in a newborn petechial rash disebabkan oleh trobositopeni,
jaundice ec hepatitis. Lesi awal dark blue to violaceous trus berubah menjadi merah/copper brown. Regress during the
first 6 weeks of life
 Bisa jg disebabkan oleh congenital rubella, toxo dan blood dyscrasia
o Keratoachantoma :
 Muir-torre syndrome associated
 Ukk : tiga tahap : proliferaitf, matur ( ada central keratotic core pada nodul sewarna kulit/ eritem, bila core diangkat
tampak crater, ada 3 bentuk ( budshape,dome shaped, dan resolving
o Cara oral kontrasepsi improve acne :
 Menurunkan kadar androgen gonadal yang diproduksi dengan cara menekan produksi LH
 Menurunkan jumlah testosterone bebas dengan cara meningkatkan produksi sex hormone binding globuline
 Menghambat aktivitas 5alfa reduktase mencegah konversi testosteron to more potent DH
 Progestin memiliki antiandrogenic effect can block androgen receptors on KC and sebocytes
o Cutaneus drug eruption dan obatnya
Erupsi makulopapular Penicilin, sulfonamid, NNRTI (nevirapin), antiepileptic
DRESS Antikonvulsan aromatic (fenitoin, fenobarbital, carbamazepin), sulfonamid, dapson, minosiklin,
alopurinol, lamotrigine
AGEP Beta lactam, makrolid , Beta blocker, ca channel blocker , anticonvulsant
Drug induced lupus Procainamid, hydralazine, isoniazid, minocyclin, acebutolol
Drug induced subacute CLE Thiazid, Ca channel blocker, ACE inhibitor
Urticarial eruption Ig e mediated hypersensitivity rx, ec penicilin,
SJS /TEN Aromatic anticonvulsants, lamotrigine, sulfonamid, alopurinol, piroxicam, dapson
Pseudoporphyria Tetracycline, furosemide, naproxen
Linear IgA disease Vancomycin, lithium, diclofenac, piroxicam, amiodarone
Pemphigus Penicilinamine, captopril, piroxicam, (thiol containing drugs) penicilin, rifampin, propanolol
Bullous pemphigoid Furosemide, penicillamine, penicilin, sulfazalasine, captopril
FDE Ibuprofen, sulfonamid, naproxen, tetracycline
 Fibroepitelioma of Pinkus :
o Untaian panjang sel basalioma yang saling bersambung dalam fibrous stroma with abundant collagen
o PA: reticulated seboroik keratosis dan superficial BCC

Palmoplantar keratoderma

Diagnosis Klinis
Huriez syndrome Keratoderma palmo plantar disertai skleroatrofi, kelainan AD, defek pada kromosom 4q23, ada
sklerodaktily / brachydaktili, predisposisi ke SCC pada usia 30-40 an
Mal de Meleda Kelainan pada mutasi ARSB gene encoding SLURP-1, mimik dermatofit superinfection. Transgredient
(extend over lateral margin of palms and proximally over the wrists)
Loricrin keratoderma Vohwinkel sindrom, khas honeycomb pattern and transgredient keratoderma, circumferential digital
involvement, cicatrizing bands, sometime autoamputation
Focal PPK Cimplicate punctate PPK in feet, srg berhub dgn nail distrofi, mutasi pada keratin 16
Punctate keratoderma Buschke fischer brauer syndrome, AD, gx: multiple keratinizing papul, berhub dgn keganasan ginjal,
gaster, mammae, colon. Kx pada gen 15q22.2 – 15q22.31
Epidermolitik Btk tersering, AD, defek pada keratin 9
keratoderma
Pachyonychia Painful focal PPK dan hipertrofik distrofi of distal nail, PC1 (Jadassohn-Lewandowsky) follikular
congenita keratosis, oral leukokeratosis dan hoarseness  mutasi KRT6A or KRT 16
PC2 multiple pilosebaceous cysts, teeth presents at birth, hair changes as protuberant eyebrows (KRT
6B or KRT17)

o Keratosis seboroik :
o Leser trelat sign: multiple eruptive SK pada keganasan t.u adenocarcinoma gaster.
o Eruptive SK pada kemoterapi dgn cytarabine
o Meyerson phenomenon: perubahan ekzematous dalam ato disekitar lesi.
o Bechet disease:
o Etiologi : genetik ( HLAb or HLA c gen, MHC class I chain A gene)
 Infeksi : virus : HSV-1, Bakteri : Streptococcus sanguinis pd oral mucosa, lipoprotein dari Mycoplasma
fermentans MALP 404)
 Autoimmune: immune mediated occlusive vasculitis autoantigen: tropomyosins dan 160 kDa polypeptide
kinectin
 Heat shock protein: 60 kDa HSP
 Cytokine: IL-1,-8, -12,-17,-23, TNF alfa meningkat, t.u IL-8 sensitive marker for disease activity
 Sel endotel: thd endotel alfa enolase, plasma endothelin-1 concentration meningkat
o PA: ada vaskulitis dan thrombosis  leukocytoclastic vaskulitis, extravasasi eritrosit, endotel swelling, neutrophilic
vasc reaction
o Terapi: bs remisi spontan, topikal: asam hialuronat0,2% gel 2x sehari, tx ulkus genital: steroid cream dan antiseptic
cream , inj triamsinolon 0,1-0,5 ml/lesi utk yg recalsitran, oral prednisone komb dgn interferon alfa, kolkisin, dapson,
cyclosporin
o Pseudopelade of Brocq :
o Primary cicatricial alopecia, footprints in the snow, bercak alopesia pada vertex dan occipital.
o PA: infiltrat limfositik yang jarang sekitar infundibulum folikular dan destruksi kelenjar sebasea, tanpa gambaran
interface dermatitis.
o Vagabond leukoderma: kondisi pada pasien dengan poor hygienic condition, abuse alcohol, infested w scabies/lice. Diffuse
lightbrown hiperpigmentasi pada pundah, pinggang, leher dan punggung : depigmented macules
o Congenital rubella syndrome :
Bila terkena dalam trimester 1: Neonatal manifestation of congenital infection
Microcephaly w mental retardation Growth retardation
Congenital heart disease (ventricular septal defect, patent Interstitial pneumonitis
ductus arteriosus, pulmonary artery stenosis)
Sensorineural deafness Radiolucent bone disease
Cataracts, Hepatosplenomegaly
Glaucoma Thrombocytopenia
Low birth weight Dermal erythropoesis “ blueberry muffin lesions”
Fetal death

 Iktiosis!!
 Acquired Ichthyosis:
o Pityriasis rotunda
o Reticulated papilomatosis of gougerot and carteaud
 Defisiensi : ADEK (fat soluble), Bcompl, C, biotin (water soluble)
Defisiensi Gejala
vitamin
A Impaired dark adaptation (nyctalopia), xerophthalmia, tumbuhnya corynebacterium xerosis pada sklrea, Bitot
spot.
Severe def corneal xerosis, ulkus, keratomalasia  perforasi kornea, prolaps iris, buta
Kulit : abN keratinisasi, mild : xerosis dan skuama, severe: fisura kulit yang dalam (dermatomalacia),
Phyrnoderma (toad skin keratotic folikular papul on anterolateral thighs and posterolateral upper arm 
meluas ke ekstensor extremitas, bahu, abdomen, punggung, pantat, wajah dan leher blkg) tp tidak spesifik, bs
ditemukan pada def vit B kompleks, vit C, vit E, Fatty acid def, PEM dan malnutrisi umum
Toxicity Vit A: dry scaly skin, with large area of desquamation and fissuring of lips and angles of mouth , tanda
awal: dryness of mouth, bs smp alopecia, follicular hiperkeratosis
Hipervitaminosis A: carotenemia
D Rickets gx skeletal, gangguan kalsifikasi tulang, rachitic rosary, scoliosis, craniotabes, lateral bowing of lower
extremites, hipotoni, fraktur, dental defek, hipocalcemic seizure (jarang)
Vit D resistant rickets tyoe II / generalized atrichia
E Jarang, bs tjd ataxia
K Impaired coagulation & hemorage pada neonatal: hemoragic disease of the newborn
Pada adults and older children: purpura, ekimosis, gingival bleeding, perdarahan GIT, genitourinary,
retroperitoneal
B1 (thiamine) Beriberi, wernicke’s encephalopathy (ophthalmoplegia, ataxia, nystagmus, laryneal nerve paralysis shg tjd
aphonia)
Dry beriberi: symmetric distal perpiheal neuropathy involving both sensory & motor system
Wet beriberi: neuropathy and signs of cardiac involvement termasuk cardiomegali, cardiomiopati, CHF, periferal
edema, takikardi, red burning tongue
B2 (riboflavin) Akut :Deep red erythema, epidermal necrolysis, mucositis
Kronik: angular stomatitis, keilosis w/ eritema, xerosis dan fisura, glositis, derm seboroik like dermatitis yg
mengenai daerah flexural of limbs and genitalia, fotofobi, konjungtivitis
B3 (niacin) Pellagra: 4D  dermatitis, diare, dementia, death.
Dermatitis: painful, eritematous, pruritic patch in photodistributed areas lm2 menjadi edem, vesikel dan bula
ruptur meninggalkan erosi berkrusta, atau membentuk skuama kecoklatanlm2 kulit menebal membentuk
plak keratotik hiperpigmentasi. Fisura yang nyeri dapat timbul di palms and soles menyerupai goose skin (glove
or gauntlet exudative crusted lesions di dorsum of hands). Butterfly distribution bs terlihat pada wajah. Kalau
dermatitis mengenai leher dan bag atas dada: Casal’s necklace, bs meluas hingga ke sternum membentuk cravat.
Mukosa yang terkena: keilitis, angular stomatitis, red tounge, ulkus pada buccal mucosa and vulva, half n half
nails.
B6 (Pyridoxine) Seboroik like dermatitis di face, scalp, neck, shoulder, pantat dan perineum
Bs ada photodermatitis, glossitis (red burning ulceration of tongue, flattening of filiform papilae), cheilitis
Neurological sign: somnolen, peripheral neuropathy, parestesia, weakness and confusion
B9 (folate) Terutama hematologi: hipersegmented neutrofil, makrositosis, anemia megaloblastik
TIDAK BERHUBUNGAN DNG GEJALA NEUROLOGIS
Gx mukokutan: glossitis dengan atrofi papila filiformis, angular cheilitis, ulserasi mukosa, perirectal ulceration,
perineal seboroik dermatitis, diffuse brown hiperpigmentation concentrated in the palmar creases and flexures
B12 Mucokutan: glossitis (Hunter’s glossitis), angular cheilitis, hair depigmentation (localized or diffuse), cutaneous
(cobalamin) hyperpigmentation (diffuse and symmetric or few scattered macules)
Berhubungan dengan subacute combined degeneration of dorsal and lateral spinal column generalized
 weakness with parestesi, ataksia, simetrik loss of vibration and proprioception, worse in the lower extremities
severe weakness, spasticity, paraplegia dan inkontinens
C Scurvy :
- kulit : follicular keratotic plugging (phyrnoderma), corkscrew hair, perifolikular purpura, lower extremity
edema with ekimosis (woody edema), poor wound healing and dehisens
- mucosa: swelling, ekimosis, bleeding of gingiva, hemoragic gingivitis, necrosis, loss of teet
- other organs: intrartikular hemoragik, suberiosteal intramuskular gangguan dari growth plate, bowing of bones,
depressed sternum, epitaksis, hematuri, GI dan cerebral hemorhage
Pelkan sign: metafisial spurs w/ marginal fraktur,
Wimberger sign: ring of increased density surrounding epiphysis
White line of Frankl : widening of zone of provisional calcification
Scurvy line/ Trummerfeld zone: transverse band of radiolucency in metaphysis
Biotin Eritematous crusting scaly dermatitis around eyes, nose, mouth and other periorificial areas
Alopecia, glossitis, conjungtivitis, irritability, lethargy, parestesi, hipotoni, developmental delay

 Porfiria cutanea tarda
o Bahan yang menyebabkan PCT: alkohol, estrogen gpada kontrasepsi/tx hormonal, hexachlorobenzene (preservative
pada gandum), tetrachlorodibenzo-p-Dioxin (toxic polutant kimiaefek : chloarcane, liver damage, hepatic phorpyria
o Etiol: gangguan sintesis heme
 Xeroderma pigmentosum
o AR, gx: kulit kering seperti perkamen, makula hiperpigmentasi freckles pada sun exposed area, gampang sunburn
o Mata: lashes rontok dan corneal keruh
o Keganasan: BCC, SCC , melanoma
 Acrodermatitis enteropathica :
o Zn deficiency, AR,
o Terjadi pada bayi yang di wean dari ASI ke sufor, atau pada bayi 4-10 minggu yg tidak ASI
o Gx: dermatitis eksim dan erosif yg simetris,, lokasi di periorificial dan akral, alopecia, diare, lethargy, irritable, whining
and crying, superinfeksi dgn C. albicans dan S. aureus
o Terapi : anak2: Zn Cl utk parenteral, elemental zinc 0,5-1,0 mg/kg dalam 1-2 dosis/ hari utk mild to moderate Zn def.
o Adult: 15-30 mg elemental zinc/hari
 Actinic prurigo
o Pruritic papul/nodul yang muncul sendiri/grup , srg ekskoriasi dan berkrusta, plak bs terdapat likenifikasi/ekzim.
o Kena sun exposed area t.u dahi, chin, cheeks, ears and forearms
o Luka yg menyembuh meninggalkan dispigmentasi dansall pitted / linear scar
 Hipohidrotic ectodermal displasia :
o Khas: rambut jarang, sulit berkeringat, kulit kering, tidak tahan udara panas, periorbital wrinkling and frontal bossing,
gigi tampak peg shaped dan sebagian ada yang tidak tumbuh
o Mutasi pada ectodysplasin pathway , NEMO, XLD
 Dermatomyositis:
o Heliotrope, gottron papul, muscle weakness!!
o PA: cell poor interface dermatitis, vasculopathy of dermal microvessels, prominent dermal mucin deposition!!
 Fifth disease :
o Nama lain: eritema infectiosum
o Penyebab: Parvovirus B19
o Khas: slapped cheek, kmdn eritem menyebar di badan, dan ekstremitas, central fading bentuk lacy/reticular,
pruritus>>
o Bs rekuren krn sunlight, exercise, temperature change, bathing, stress
o Sembuh sendiri dlm 1 -2 minggu
Kosme:
 Aza: comedolytic n antimicrobial property  safe in pregnancy
 SA: komedolitik & exofiliation of str corneum
 Sulfur/resorcinol : inhibit PABA shg P acne ga bs tumbuh , srg combine dgn sodium sulfacetamid
 BPO : antimicrobial agent
 Tret: comedolytic n anti-inflamm
 Tetra: doesn’t alter sebum production, decrease conc of FFA, esterified FA meningkat
 Spironolacton: reduce sebum production
 Acute hemorrhagic edema of infancy
 Mirip HSP, tp kena anak < 2 tahun,
 Gx: painful edematous petechiae and ekimosis kena daerah kepala dan bagian distal ekstremitas. Facial edema
earliest sign.
 Skin lesion: target like appearance, bs tbtk bula & nekrosis.
 Pencetus: imunisasi, infeksi, obat2
 Beda dgn HSP: AHEI ini pada anak 4 bln – 2tahun, lack of systemic features, resolusi dalam 1-3 mgg tanpa gejala
 Tx: AH1
 Scarlet fever
  Streptococcal: white strawberry tounge 2 hari pertama, kmdn deskuamasi menjadi red strawberry tounge 2 hari
berikutnya
 Staphyloccocal: tidak ada pharingitis nya!!!
 Kontraindikasi vaksin zoster
 Px dgn leukemia, limfoma, ato keganasan lain yg mempengaruhi bone marrow/limfatik sistem
 AIDS dgn CD4 ≤ 200 &/ ≤15% total limfosit
 Px dgn tx imunosupresif: high dose CS tx (20 mg/hari atau lebih prednison selama 14 hari atau lebih
 Low dose Mtx (≤0,4 mg/kg/mgg), azathioprine (≤ 3,0 mg/kg/hari) or 6-mercaptopurine (≤1,5mg/kg/hari)  bukan
kontrainidikasi absolut
 Giannoti crosti syndrome:
 kena anak2, 6-12 tahun, sembuh sendiri dan asimtomatik, kdg ada limfadenopati
 ukk: papul monomorf, flat topped, dome shaped, eritem pada muka dan limbs
 dipicu oleh EBV, vaksin, bs jg CMV, enterovirus, respiratory syncytial virus, rotavirus, adenovirus, echovirus, pox,
polio, etc etc
 sembuh sendiri, tp bs kasih steroid topikal potensi sedang
 EBV mononucleosis:
 Copper colored papules on trunk & extremitas
 Atipikal limfosit!!
 Exanthema subitum
 = roseola infantum ,
 ukk: palpebral edema (tampak ngantuk) yg hilang sendiri sehari setlah exanthem. Papul eritem pada soft palate
(nagayama spot) muncul sbelum viral exanthem khasl: rose red macules/papul 2-5 mm surrounded by white halo
 Erisipeloid:
 Kerja di bagian fishing/ animal product
 Inkubasi 2-7 hari
 Gx awal: nyeri pada lokasi yang terkena, kmdn terbentuk plak dermal keunguan. Batas tegas, limfangitis dan regional
adenopati muncul, low grade fever, malaise
 UKK khas: keunguan yg hangat pada tangan , well defined raised margin with anular/polygonal border, srg mengenai
sela jari2, spare terminal phalanges, does not progress beyond wrist!!
 Dpt sembuh sendiri dalam 3 minggu
 Osler node:
 erythematous or hemorrhagic macules, papules or nodul very painful / tender , located distally on digital tufts
 PA: perivasculitis or necrotizing vasculitis without microabses formation or other evidence of infetion or emboli
 Janeway lesion
 Eritematous or hemorhagic macules, papules or nodules NON TENDER!!! Located on palms and soles
 PA: vasculitis WITH microabses formation!
 Osler n janeway: ditemui pada bacetrial endocarditis, sle, gonococcemia, anemia hemolitik , typhoid fever
 Livedoid vasculopathy
 Nama lain: livedoid vasculitis, atrophie blanche ( porcelain white atrophy, telangiectasis dan ulkus end stage of
vascular damage in skin )
 Biasa tjd pada px dgn kx connective tissue: SLE, malignanty condition, hypercoagulable state, thrombophilia, idiopathic
disorder,
 Bs tdp def Protein C dan S, mutasii faktor V leiden gen, aktivated protein C resistance, prothrombin gene mutation,
hyperhomocysteinemia, antithrombin deficiency, Antiphospolipid antibodi bs (+)
 Sneddon syndrome: livedoid racemosa dan livedoid vaskulitis berhub dgn iskemik cerebrovasc lesions, hipotensi,
extracerebral arterial dan venous thromboses. Antiendotelial cell antibody terdeteksi di serum, antiphospholipid
antibodi, anti β2 glikoprotein antibodies dan antiprothrombin antibodies bs positif!
 Livedo racemosa:
 Ada vasospasme arteriol yg lama, trombosis dan atau hiperviskositas
 Antioksidan enzimatik: SOD, catalase, glutation peroksidase
 Antioksidan nonenzimatik: Vit E, coenzyme Q10, ascorbat, carotenoids
 
 Eosinofilik pustular folikulitis
 Ada 3 tipe: ofuji disease, yg berhub dgn imunosupresi, pada bayi/neonatal
 Ofuji disease: pada px jepang, dgn pustul folikuler kronik rekuren, membentuk plak circinate, distribusi seboroik
 g berhub dgn imunosupresi: plg srg pd px HIV, severely pruritic papul pada face dan upper trunk
 Pd bayi/neonatal: follicular pustules of the scalp
 Khas: folikular and perifolikular eosinophil infiltration
 Berhub dgn peripheral blood eosinofilia
 Bs rekuren dan kronis kec pd bayi
 Calcifilaksis:
 Life threatening, adanya progresif vascular kalsifikasi, soft tissue necrosis dan iskemik nekrosis pada kulit.
 Bisa muncul dimana saja, tp lower extremity >>>, mortality rate tinggi
 PA: medial calcification of small and med size arteries with intimal hyperplasia primarily in dermal and subQ
 Terutama muncul pd px gagal ginjal kronis dan prolonged secondary hyperparathyroidism
 Bs berhub dgn obesitas dan poor nutrition
 Lbh srg pada perempuan>>>
 Glucocorticoid:
 Metabolisme meningkat bila kombinasi dgn: rifampicin, barbiturat, fenitoin  smua menginduksi hepatic microsomal
enzyme
 Penyerapan steroid tgg bila dicampur dgn cholestyramine, colestipol dan antasid.
 Warfarin + Glucocorticoid: dosis warfarin butuh lbh tinggi utk antikoagulasi
 Glucocorticoid menurunkan kadar salisilat serum
 Mengganggu delayed type Hypersensititivity
 Heerfordt syndrome:
 Fever, parotid gland enlargement, facial palsy, anterior uveitis , bs tjd pada sarcoidsosis
 Schamberg disease:
 ukk: reddish brown patches with pin head sized reddish puncta resembling grains of cayenne pepper. Bisa multiple,
diskret, confluent nonpalpable, nonblanching purpuric lesion of many months duration on legs. Acute microhemorhages
resolve with deposition of hemosiderin  membentuk dark brown peppered stain
 itrakonazol absorbsinya akan turun bila diberikan bersamaan dgn H2 blocker (terfenadine), antacid dan PPI
 itrakonazole ga boleh dikasih barengan dengan: Cisapride, terfenadine, quinidine, dofetilide, oral midazolam, pimozide, triazolam
 azole eksresi dalam ASI.
 fluconazole: fungistatik, tidak efektif untuk C. krusei
 Twenty nail syndrome (trachyonychia) bisa ada pada alopecia areata, liken planus, psoriasis, eczema
 Yellow nail syndrome: rrespiratory disorders, rheumatoid arthritis, internal malignancies  tx dgn high oral dose of vit E , bs
sembuh spontan, topical vit E dan tx antifungal sistemik gak efektif !
 Obat2 yg memicu eksaserbasi psoriasis:
o Beta blocker, antimalaria , lithium, NSAID, IFN alfa dan gamma, imiquimod, ACE inhibitor, gemfibrozil (LAMBE
INAGI)
 Felty syndrome: suatu ulkus refrakter pada kaki pasien dgn reumatoid artritis dan hipersplenism. Serum reumatoid meningkat,
ada pembesaran limfe. Radiologi: kalsifikasi tulang berbatasnya tegas dan sebagian besar ditandai erosi berdampingan pada
sendi.
 Pertumbuhan kuku tangan komplit : 100-180 hari (6 bln), kalo nail plate di ekstraksi, butuh 40 hari sebelum kuku baru muncul
dari proksimal nailfold, dlm 120 hari akan mencapai fingertip. Total regenerasi utk kuku kaki: 12-18 bulan!!!
 Lofgren syndrome:
o Eritema nodosum disertai bilateral hilar adenopati, arthralgia, dan fever gx awal sarcoidosis
 DKA:
o Purpuric ACD: pada lower legs and/feet, t.u karena textile dyes
o Lichenoid ACD: rare, menyerupai liken planus, berhub dgn metallic dyes in tato, oral lichenoid ACD krn dental
amalgam jg bs menyerupai oral lichen planus
o Pigmented ACD: bnyk pada Asia
o Limfomatoid ACD: berdasarkan histoPA saja!! (adanya significant dermal infiltrate displaying features of
pseudolymphoma), gx klinis ga spesifik. Termasuk alergi thd metal, hair dye, dimethylfumarat
 Ainhum: (dactylolysis spontanea)
o Etiol: chronic trauma, infeksi, hiperkeratosis, decreased vascular supply, impairede sensation produce eksesif
fibroplasia
Iktiosis vulgaris - Autosomal semi dominan
- iktiosis yang plg sering, cukup ringan
- gejala srg muncul dalam 1 tahun perama
- skuama prominent pada permukaan ekstensor dari ekstremitas, flexural sparing!! Diaper area spared
- lower extremities plg severely involved, skuama centrally attached dengan “cracking” pada bagian tepi.
- Hiperlinearitas palmar , keratosis pilaris is common, biasanya melibatkan tangan bagian luar, extensor paha
dan pantat,
- Atopi +, hay fever, eczema atau asma
- Hipohidrosis dgn heat intolerance  memburuk pada cuaca dingin dan kering, membaik pada lingkungan
lembab dan hangat
- Mutasi : pada profilaggrin (protein prekursor dari filaggrin, yg berfx saat kornifikasi
- PA: hiperkeratosis, granular layer absent!!!
X-linked recessive - pada laki2, aktifitas enzim steroid sulfatase menurun/ hilang pada epidermis, str corneum, leukosit dan
ichtyosis (XLRI) fibroblast. Terjadi penumpukan kolesterol sulfat pada serum dan skuama dan epidermis , increased mobility
of β-lipoprotein pada elektroforesis dpt sebagai diagnosis
- skuama mulai pada periode newborn, most prominent pada permukaan extensor, flexural area terlibat!
- Severe involvement w/ skuama besar2, comma shaped corneal opacities pada pasien dewasa
- Risiko cryptorchidism meningkat, increased risk of testicular cancer
- PA: compact orthohyperkeratosis, akantosis dan papilomatosis, lapisan granular menebal !!
- Kelainan pada kromosom Xp22, delesi pada mutasi ini bs dideteksi dengan FISH (fluoresen in situ
hybridization)
- Bila delesi tidak terdeteksi, bs diukur kadar enzim arylsulfatase C (steroid sulfatase) pada fibroblas kultur
- Bs overlap dengan kondrodisplasia punctata
- Kallman n syndrome (hipogonadotropic hipogonadism dan anosmia), renal abnormality, obesity, synkinesis
, cleft palate and spastic paraplegia  bs berhubungan deng XLRI
Autosomal recessive - ada saat lahir, generalized involvement of skin.
congenital ichthyosis - LI: large dark plate-like scales, infants may be red at birth, adult no erythroderma
(ARCI)- - Severe case: bs ektropion dan eklabium, scarring alopecia ec traction at hairline
- Pasien kongenital ichtyosiform eritroderma : have little to no ectropion, eclabium or alopecia.
- Autosomal recessive pattern
Lamellar ichthyosis - present at birth, newborn pny collodion membrane, skin may be red, lama2 muncul skuama besar plate-like
yang berpola mosaik. Skuama melekat ditengah dengan tepi bebas, skuama terbesar pada ekstremitas
bawah , antar skuama ada fissura, keterlibatan palm n soles variable, dari minimal hiperlinearity to severe
keratoderma
- lips and mucous membrane spared!!, adnexal structure compromised by adherent firm scales
- scarring alopecia at the perifer of scalp
- severe heat intolerance,
- can treat w oral retinoid can improve or prevent some sequeale of LI  dpt menurunkan thick periocular
scale, mengurangi ectropion
- PA: orthokeratotic hyperkeratosis w/ mild to moderate akantosis, rate of epidermal proliferation are normal
or only slightly elevated in px with LI
- Mutasi pada TGM1
- Bathing suit ichthyosis: bentuk unusual, individu yg terkena develop scaling typical of LI tp limited to
bathing suit area.
Collodion baby - Bayi lahir dgn collodion membrane, bs mild to severe,
- Biasanya bayi prematur,
- Pada 2 minggu pertama kehidupan, membran pecah dan mengelupas, meninggalkan fisura, ganggauan thd
barier shg muda infeksi dan water loss  increased infection, difficulties in thermal regulation,
hypernatremic dehydration . kulit yang mengelupas kalo dibiarkan kering bs mengeras menimbulkan
konstriksi shg jd bengkak
- Tx: humidified incubator, wet compresses, blanc lubricants
- Usual presentation of ARCI , AR
Harlequin ichthyosis - Severe, fatal form of ichthyosis
- Premature child, born with massive shiny plates of str corneum separated by deep red fissures, tend to form
geometric patterns
- Poorly developed or absent ears and marked ectropion and eclabium
- At great risk during neonatal period, srg meninggal segera setelah lahir,
- Risk of fluid and electrolyte imbalance, risk of infection,
- No normal lamellar granules!!! Tp ada small vesicles with no internal structure
- Autosomal recessive : ABCA12
KLASIFIKASI EB
Level of Disease Defect Keterangan
separation
Simplex Generalized KRT5/KRT14 Koebner EBS, onset at birth/early infancy,
Kena hands, feet, extremities, lesi sembuh dgn hipo/hiperpigmentasi,
Oral mucosa bs terlibat w/ mild erosion
Simplex Dowling-Meara KRT5/KRT14 The most severe, oral mucosa srg terkena, spontaneous appearance
of grouped/herpetiform blisters di extremitas dan trunk, heal w/o
scars, milia (+), nail involvement (+)
Simplex Localized KRT5/KRT14 Mildest form, Weber-Cockayne subtype, bentuk tersering!!muncul
saat infancy/childhood. Srg berhub. Dgn hiperhidrosis palm n soles.
Milia n scar (-)!!!, blister muncul pd daerah trauma
Simplex Ogna KRT5/KRT14/PLEC1 Common onset in infant, t.u saat summer on acral areas. Khas!
Onychogryphosis of great toenails
Simplex Mottled KRT5/KRT14 Mottled hiperpigmentation of trunk& proximal extremities, pigment
Pigmentation alteration appear reticulated, increase with age
Simplex EB w/ muscular PLEC1 Rare, blistering generalized at birth/segera sesudah., mutasi
dystrophy plectin/HD1
Simplex Superficialis KRT5/KRT14 Suprabasal EBS, subcorneal separation!!sering ditemukan erosi &
krusta
Lethal acantholytic EBS: nails dystrophic – absent, complete
alopecia, neonatal teeth, oral erosions, repsiratory involvement

Simplex Ectodermal PKP1 Ectodermal dysplasia skin fragility syndrome: supra basilar
dysplasia-skin epidermal separations khas! Generalized erosion and alopecia,
fragility palmoplantar keratoderma, painful fissures and nail dystrophy.
Junctional EB w/ pyloric ITGB4/ITGA6/PLEC1 Extreme mucosa & cutaneous fragility, w/ various urological
atresias abnormalities. Mutasi pada gen coding β4 & α6 integrin!
Junctional Herlitz LAMB3/LAMA3/LAMI2 JEB letalis, bentuk severe, lethal: widespread blistering at birth. Nail
involvement w/ periungual hipertrofik granulation tissue during
neonatal period!! Suara serak saat bayi, gagal tumbuh dan growth
retardation!!involvement of large airways, nail severely affected, lost
during infancy
Junctional Non Herlitz LAMB3/LAMA3/LAMG2 Loss of nail and skin atrophy! Scalp and nail lesions , periorificial
/COL17A nonhealing erosions w/ granulation
Junctional Localized COL17A1 = minimus JEB, rare, accentuated in localized areas, plg srg tangan,
kaki, pretibia. Absence of any internal involvement
Dystrophic Generalized COL7A1 Pasini subtype, more severe & widespread blister, spontaneous
dominant appearance of distinctive scar-like flesh colored papules on trunk
Dystrophic Localized COL7A1 Cockayne-Touraine of DDEB, kena daerah trauma sperti knee,
dominant sacrum & acral
Scar is often hipertrophic, milia (+) , nail abnormality (+) , oral
lesion not common, teeth unaffected
Dystrophic Recessive COL7A1 Mild : RDEB mitis, mucosal involvement mild,
Severe: Hallopeau Siemens: generalized blistering at birth, extensive
denudation of entire region of skin at birth, mengenai salah satu
limb Bart’s syndrome, pseudosyndactyly (+) , no periorifical
involvement , bs mjd keganasan
Variable Kindler KiND1 EB like trauma induced blistering at birth & during infancy, w/
syndrome atrophic changes during healing seperti JEB/DEB
EBS: BP230 dan lamina densa protein sperti kolagen tipe 4 ada pada dasar bula
Junctional: blistern formation in lamina lucida of BMZ krn defek anchoring filament yg terletak di lamina lucida dan superior lamina
densa. BP230 ada pada atap bula, kolagen tipe 4 pada dasar bula
Dystrophic EB: EB heal w/ scar and milium formation!! Bentuk recessive have increased prevalence of invasive SCC. BP230 dan
kolagen 7 ada pada atap bula. Bila pada pengecatan, tidak ada kolagen 17  nonherlitz JEB/ generalized atrophic benign EB.
 Diagnosis Gejala Histo PA
ACLE Bs localized to face : classic butterfly/malar rash. Nasolabial fold limfoshistiositik infiltrat jarang, mild
is spared!! degree of focal vacuolar alteration of
Generalized ACLE: morbiliform eruption on extensor : arm dan basal KC, bs ada necrotic KC, upper
hands knuckles are spared!!! Predominant on sun exposed skin, dermis pronounced mucinosis.
t.u lbh srg kena daerah malar
Sering berhubungan dgn SLE  titer ANA, anti-dsDNA, anti-
Sm, and hypocomplementemia tinggi
SCLE Ada Ro/SS-A ribonucleoprotein particle (70%-90%) anti La/SS-B Interface dermatitis, foci of vacuolar
(30-50%) , ANA : 60-80%, Rheumatoid factor di 1/3 alteration of basal KC alternating w/
Gx: makula/papula eritem jd plak hiperkeratotik area of lichenoid dermatitis.
anular/polisiklik, lbh srg pada lateral wajah, malar tidak terkena, Dermal changes: edema,prominent
lbh srg pada leher, bahu, extrem atas dan trunkus mucin deposition, sparse mononuclear
Muncul di daerah sun exposed, heal tanpa scar cell infiltration limited to around BC
SCLE: bs VDRL false positif, anticardiolipin, antitiroid, anti Sm, and periadnexal structures, dermal
anti dsDNA, anti U1 ribonucleoprotein. melanophages!!!
SCLE bs pny lab abnormality sperti SLE IF: IgG deposit pada lapisan basal
menyerupai dust like particle
DLE Awal: red purple makula, papul/ small plak yg dgn cepat memiliki Hiperkeratosis epidermis, atrofi dan
permukaan hiperkeratotik, berbatas tegas, coin-shaped. Atrophic interface changes. Epidermal BMZ is
central scarring. Scaring alopecia! Folicular involvement (Carpet thickened.
tack sign)!! Srg pada scalp, face, ears (t.u bag external), Dermal changes: dense mononuclear
Nasolabial fold spared! Localized DLE: only in head/neck, tp infiltrat tdd limfosit dan makrofag t.u
gener pada daerah periappendageal dan
ANA bs (+) low titer, anti ssDNA sering, to anti dsDNA jarang!!! perivaskular, melanophages, & dermal
Ro/SS-A dan La/SS-B jarang pd pasien DLE mucin deposition.
Bs VDRL false positif, RF test (+), leukopenia, modest elevation Infiltrat bs smp ke deep reticular dermis/
in γ globulin, modest leukopenia  predictor utk SLE subcutis
ANA : (+) pada 70-75% px LE profundus/paniculitis tapi anti
dsDNA antibody jarang.
Chilblain  Purple red patch, papul, plaq on toes, finger, face
LE  Krn udara dingin/ lembab
 Scarred atrophic plak dgn teleangiektasis,
 Adanya superficial dan deep limfositic vascular
reaction , fibrin deposision in rreticular, dermal based
blood vessels.
Associated w/ anti Ro/SS-A antibodies, mutasi TREX1 gen
LE Variant CCLE dgn dermal finding of DLE, excessive mucin
tumidus deposition and superficial perivascular and periadnexal
inflammation, gejala annular urticaria-like plak. ANA test (-), the
most photosensitive CLE
Teleskopi finger: krn resorbsi tulang pada MH, kalo mutilasi : karena nekrosis tulang2

Tanda awal melanoma: perubahan warna dan peningkatan ukuran, gatal jg tp tidak spesifik
X-Linked Dominan X-Linked Resesif Autosomal resesif Autosomal Dominan Autosomal semi Dominan
IP X-linked Recessif XP TSC Icthyosis vulgaris?
ichthyosis
CHILD syndrome Wiskott Aldrich Cockayne syndrome NF1/2
syndrome
Bazex Hypohidrotic Bloom syndrome Huriez syndrome
ectodermal dysplasia
Conradi hunermann ARCI/LI Ichthyosis vulgaris
happle (XLD
chondrodysplasia
punctata)
Harlequin ichthyosis Ichthyosis bullosa
Siemens
Netherton syndrome Ichthyosis hystrix
KID sndrome
Chronic candidiasis
w/o endokrinopati
Darier
Hailey2
 Jamur 03/05/2017 22:29:00
 Bentuk2 jamur dalam SDA :
- Epidermophyton floccosum : club-shaped macroconidia
- Microsporum audouinii : pectinate (comb like ) hyphae & terminal chlamydoconidia
- M. canis : thick walled echinulate spindle shaped macroconidia with terminal knobs
- M. gypseum : thin walled pickle shaped macroconidia w/o knobs
- T. interdigitale : grape like clusters of round microconidia, rare cigar-shaped macroconidia, spiral hyphae. Hair
perforation (+)  beda dgn T. rubrum. Warna putih kuning beludru, warna bisa light brown
- T. rubrum : tear-shaped microconidia, rare pencil shaped macroconidia. Hair perforation (-),warna maroon , cherry red
on PDA
- T. schoenleinii : knobby antler like hyphae (favic chandeliers), chlamydoconidia banyak , colorless to yellow tan
- T. tonsurans : multiform microconidia, cigar –shaped macroconidia , maroon or white to yellow color
- T. verrucosum : chains of chlamydoconidia, long and thin “ rat tail” macroconidia with thiamine , white to yellow gray
- T. violaceum : iregular hyphae w/ intercalary chlamydoconidia. Purplish red
-
 MH cacat derajat 2:
 Lagoftalmus
 Kekeruhan kornea,
 Kemerahan yang jelas pada mata ec ulserasi kornea / uveitis
 Gangguan penglihatan berat/ kebutaan
 Luka dan ulkus di telapak
 Deformitas ec kelumpuhan otot, atau hilangnya jaringan atau reabsorbsi parsial jari
 Teknik 03/05/2017 22:29:00
 Filler: HA
 Nasolabial fold: serial threading trus cross hatch at right angle
 Cheek : deep bolus injection
 Lip: depot or threading technique
 Suborbital hollow: depot or threading
 Sub-brow area: push ahead technique
 Filler PLLA:
 Diffuse crosshatching and threading  depot is no longer recommended
 Lower face: linear threads each 0,1 ml , 2 mm apart , injeksi subdermal
 Upperface: diffuse threading 0,05 ml PLLA under or close to periosteum
 Komplikasi: palpable papul formation
 Utk tx lipoatrofi berhub dgn HIV
 Filler Ca Hidroxiapatite
 Threading technique, infiltration at dermal-subcutaneous junction for nasolabial fold
 Deep fat or supraperiosteal region in cheek and mandible
 Utk atrofik acne scar, recontour nasal defect, nipple reconstruction
 Komplikasi: Nodul CaHA di lips
 Filler autologus fat:
 Filler utk collagen vascular disease, or yg allergi to collagens or hyaluronic
 Flap :
 H- plasty : forehead and upper lip , = bilateral U plasty
 O-T flap or A-T plasty : bagus utk daerah dengan dasar lebar along a free margin or cosmetic unit junction : eg lip or
eyebrow
 Crescentic advancement flap: bagus utk repair upper lip dan perialar defect
 Island pedicle flap or V-Y flap : utk nasal dan perioral closure eg: superior nasal tip, superior or lateral vermilion border,
to help avoid distortion of the area around defect.
 Rieger flap : repair nasal defect involving distal dorsum or tip
 Bilobed transposition flap: utk small to medium sized defects of lower nose, preventing distortion of the alar rim
 Injeksi Botox:
 Glabelar brow furrows:  eyelid pstosis
o Suntik 20-35 unit botox/ xeo min atau 50-75 unit dysport dalam 5 lokasi berbeda utk terapi otot corrugator dan
procerus in brow
o Injeksi corrugator: 1. Just at or above medial brow and 2. Just medial to midpupillary line, at least 1 cm above
bony orbital rim  to reduce ptosis
o 5th injection is placed in the procerus at the midline above the horizontal creases created in glabella at the brigd
of the nose
 Horizontal forhead line: koreksi frontalis muscle
o Suntik 12-20 unit BOTOX or 20-50 unit Dysport dalam 4-5 dosis terbagi along the forhead equator
 brow ptosis: krn overzealous tx of frontalis muscle  dosis terlalu besar atau injection site too low
 transient lid edema : krn periocular injections
 headache: upper third of face
 crow’s feet: suntik approximately 1 cm lateral to the lateral canthus dibagi 1-3 titik, dosis 10-18 unit botox, or 25-30 unit
Dysport
 hiperhidrosis axilla : 2,5-4 unit botox tiap 1-2 cm di axilla. Anhidrosis bs bertaham 8-12 bulan
 palmar hiperhidrosis : anestesi pake regional wirst block, dgn 1-2% lidocain tanpa epinefrin. Suntik 100-150 unit botox
utk setiap palmar. Dibagi menjadi 2-3 unit injeksi sebanyak 50-60 intradermal injection
 Laser:
 Untuk nevus Ota & pigmentasi krn obat2: Q-switch laser , Qs ruby
 Untuk PWS & hemangioma,: PDL , nodular PWS: continous wave CO2
 Utk teleangiectasis: PDL dan IPL , KTP, diode laser / NdYag
 Lentigines: Qs ruby, Qs NdYAG 532/1064, Qs alexandrite
 Varises: PDL, alexandrite
 Cherry angioma” KTP dan PDL
 Small angiorfibroma : KTP
 Xanthelasma dan syringoma: KTP CO2
 Tricoepitelioma: Co2, ErYag,
 Neurofibroma : Co2 laser
 Eruptive vellus hair cyst: Co2
 Veruccous epidermal nevi: Co2, KTP laser, ERYag
 Sebaceous nevi:CO2 dan ErYAG
 Kondiloma/kutil, : CO2, HIV(+): NdYAG
 Moluscum: PDL
  Rosacea: PDL
 Vitiligo: ErYAg, Excimer
 Keloid: PDL, CO2,
 Psoriasis: laser excimer
 Untuk hair epilation: alexandrite, diode Pulsed NdYAG (fewest side effect), IPL
 Acne scar : Er /yag or CO2 dgn flash scanner
 Lentigines: QS ruby, QS NdYag, Qs Alexandrit
 Tato black blue: NDYag 1064
 Tato: blue black green : Q-switched ruby and alexandrite
 Tato : red: short pulsed dye 510 nm dan Q-switched 532 nm NDYAG
 Yellow: resistant to laser tx!!!
Excimer: target DNA lesion
Qs Ruby PDL (585) NdYAG Alexandr KTP CO2 ErYag Excim IPL Diode
532/1064 ite er 308
755
Nevus PWS Pulsed PWS PWS risk Nodular PWS tricoepitelio vitiligo PWS Veno
Ota 1064: PWS deeper scar besar : yg continous ma us
deeper vessel CO2 lakes
vessel
Pigment Hemangio Teleangiecta Starburst teleangiecta tricoepitelioma Epidermal Psorias teleangiecta acne
asi obat ma small sis veins sis nevi soft is sis yg
diameter<1 papilomatos berkelompo
mm  a k
scar>>
lentigine teleangiecta starburst epilation xanthelasm Neurofibroma xanthelasma alopeci Poikiloder
s sis veins for dark a/ / syrngoma a ma of
skin syrngoma areata Civatte
Nevus Cherry Low flow Tato: Cherry Eruptive Sebaceous Striae
ota, angioma venous malf black angioma vellus hair cyst nevi distensae
nevus of blue
ito green
Tatoo: Venous Venous Venous Digital Kondiloma
black, lakes lakes lakes mucous cyst  best utk
blue yg flat
black,
dark
blue
green
pruritus komdil pada Epidermal ILVEN/ hard Hailey-
pada px HIV nevi soft verucous nevi hailey
ILVEN papilomato
sa
Molluscum Pulsed Sebaceous Vitiligo
NdYAg nevi
1064
Rosacea lentigines condyloma Acne skar
hipertropik 532: Red boweinoid
skar / tato papulosis
keloid 1064 : black
blue tato
veruka
liken sklerosus
chondrodermat
itis nodularis
helicis
Hailey2

 Tissue  Vascular  Pigmented  DNA protein

Argon Argon NdYAG 532 Excimer (XeCL) 308
Flash lamp pulse dye NdYAG 532nm Ruby 694
Diode 810 KTP laser Alexandrite 755
Diode 1450 Flash lamp pulse dye 585- NdYAG 1064
600
ErYAG 2960 Alexandrite 755
CO2 10600 Diode 810
Aleandrite 755 NdYAG 1064
 Dermabrasi:
 Pear shaped fraises and cones  utk daerah hidung dan oral commisures
 Wheels: flat, broad skin surfaces
 Diamond greater safety than wire
 Anestesi; bs pake tumesen anestesi for full face dermabrasion (250-350 cc utk 1 wajah)
Cryosurgery: clinical freeze margin: lesi jinak: 2-3 mm, lesi ganas: 5 mm

3-5 5-10 8-10 10-15 30 30-60 60

Solar lentigo Seb hiperplasia Aktinik keratosis KS Keloid & skar Lentigo maligna dermatofibroma
hipertropi
Bowen disease

Nervus damage: pada digital block

Alopecia: bila freeze time 20 detik
Scar: bila suhu -20-35

Utk hair removal: elektrolisis

Utk pasien dgn pacemaker ato defib (ICD) : elektrokauter
Bovie knife: elektrosection


 Sifilis -HOLMES 03/05/2017 22:29:00
 Proses perlekatan T. pallidum pada fibronektin sel pejamu diperankan oleh gen Tp0155, Tp0483
 Early syphilis :
 Bakteria masuk melalui permukaan mukosa yg utuh atau via microscopic abrasion in skin multiply locally (selama 30
jam). Dalam waktu jam pertama hingga bbrp hari setelah infeksi  organisme mampu masuk ke sirkulasi (termasuk
limfatik) dan menyebar luas termsk ke CNS dan fetus
 Chancre: lesi primer, muncul pada lokasi infeksi, disebabkan oleh host’s cellular infiltration triggered by adanya
treponema dalam jumlah banyak. Regional bilateral limfadenopati seirng. Lesi sembuh sendiri dan individu yang
untreated may manifest the 2ndary stage after weeks to –months
 Sifilis sekunder:
 Lesi kulit (maculopapular rash) on trunk, extremities, palms and soles, mucous membr lesions and hypertrophic lesions
in moist body crevices (condylomata lata) srg disertai sistemik limfadenopati
 Bisa sembuh sendiri krn imun response host
 Gx lain yg jarang dan signs of 2ndary sifilis: alopecia, subclinical or clinically apparent hepatitis, uveitis,
symptomatic/asymptomatic CNS involvement
 Resolusi  masuk ke latent stage
 Lesi 2nder bs muncul lagi t.u tahun 1 infeksi
 Early latent syphilis: sifilis < 1 tahun , late latent > 1 tahun
 Sifilis tersier
o Gumma
o Cardiovascular involvement (aortitis, aortic aneurysm),
o Or symptomatic late neurosyphilis (tabes dorsalis, paresis, optic athropy)
o Acute syphilitic meningitis:
 Masa inkubasi satu tahun, masih ada rash sekunder saat meningitis, bisa ada cranial nerve palsy dan tanda2
increased intracranial pressure.
 Lab: CSF: elevated pressure, pleositosis mononuklear (10-200cell/mm3 atau bs sampe 1000-2000 cell per
mm3), peningkatan kadar protein (bs sampe 200 mg/dl), VDRL pada CSF reaktif
o Meningovascular syphilis:
 Infark sekunder to syphilitic endarteritis  muncul 5-12 tahun stelah infeksi sifilis awal
 Gx: ada hemiparesis/hemiplegi, afasia, seizure. Yg sering terlibat adalah a. serebri media.
o Cardiovascular syphilis: paling sering kena aorta asending !!!, aneurisma aorta torakalis
 Mekanisme invasi:
o Fibronectin and laminin may play a role dalam kemampuan T. pallidum utk diseminasi
o Laminin banyak di bawah endotel dan sel epitel  T pallidum bind to laminin, may facilitate intial inf through the
epithelial surface and dissemination by guiding bacterial migration into the vasculature
o T. pallidum tidak pny LPS jd tidak mengaktivasi sel melalui TLR4, tapi lipid portion of treponemal lipoproteins (Tp47,
Tp15, Tp17) serve to activate cells through TLR2/1 heterodimers tapi lipoprotein ini gak ada di permukaan T.
pallidum  shg bs escape immediate detection by innate immune system bs multiplikasi dan diseminasi
o Beberapa teori persistensi sifilis:
 Lokalisasi dalam sel host
 Masquerading by coating bacterial surface with host protein
 Relative lack of surface exposed protein antigens  major factor!
o Specific/ generalized immunosuppresion
 Hoigine rx: rx psikotik akut akibat prokain dalam penisilin , bukan reaksi alergi
 Penurunan titer 4x dari yang sebelumnya tidak perlu diobati, tapi diulang lagi 1,3,6,9 bulan, 1 tahun, 2 tahun kmdn
 Terapi sifilis primer:
 2,4 juta IU benzathin penisilin SD
 kalo ga bs penisilin : ceftri 1 g iv/im tiap hari 10 hari
 Penpro 600.000 IU im selama 14 hari
 Tetracycline 500 mg 4x1 or doksi 100 mg 2x1 14 hari
 Pasien gagal tx: diukur dgn clinical relapse/ 4x lipat peningkatan RPR harus di retreated dgn benzatin penicilin dosis
2,4IU i.m weekly for 3 weeks.  sama dgn tx late latent sifilis
 E.s : chills, fever , artharlgia, headache, dan transiently increased prominence of lesions  Jarisch Herxheimer rx 
akibat penggunaan penisilin hny diberi obat simtomatik, tidak perlu menghentikan obat, merupakan terapi associated
response, bukan drug hipersensitivitas reaction, ada peningkatan TNF alfa
 Neurosifilis: Benzatin penisilin 18-24 juta unit setiap hari selama 10-14 hari atau inj im procain penisilin G 2,4 juta unit
+ probenecid 500 mg po 4x sehari selama 10-14 hari.
 Lesi Corymbose: flat topped flower bouquet lesions appear as a central large papule or nodule surrounded by small satellite
papules masuk dlm bagian sifilis sekunder papular (H1182)
 Terapi sifilis: 1: 4 sudah di terapi
 Risiko neurosifilis pada pasien HIV meningkat bila RPR > 1/32 atau CD4 < 350
 Late benign syphilis or gumma is a proliferative granulomatous inflammatory process that may be destructive of affected
tissues
 Sifilis belajar titer, reaksi dan terapi!!!
 VDRL false positif pada apa? Human eror, alat eror, ibu hamil, peny autoimun t.u SLE ,  VDRL positif tu harus ditentukan
penyebabnya apa? Terbanyak memang karena sifilis
 Early congenital sifilis :
o Terjadi dalam 2 tahun pertama kehidupan
o Snuffles,
o Palmar and plantar bullae  Pmphigus syphiliticus
o Splenomegaly
o Syphilitic nephrotic syndrome
o Syphilitc leptomeningitis
o Ocular syphilis: syphilitic chorioretinitis : salt and pepper pattenr of pigmentary patches at the perifer of granular
fundus,
o Pseudoparalysis of Parrot: epifisitis of radius, femur humerus dan fibula.
o Cutaneous syphilids 
o corymbiform lesions of grouped papule around large central plaque like hen and chicks!
o Paronychia
o Rhagades : fisura sekitar nares lips dan anus
o Eritematous makula dan papul dengan skuama, eritema dan deskuamasi pada daerah perioral
 Late congenital syphilis
o Bisa terjadi pada adolesent  not infectious
o Stigmata / malformasi : high cranium / tower skull , muka terlihat flat dengan saddle nose deformity
o Higoumenaki sign : penebalan clavicula pada 1/3 medial pada sisi tangan dominan
o Gigi : moon molar seperti mulberry, bouton de fleur, cow’s udder atau string purse
o Interstisial keratitis  salah satu triad hutchinson
o Rosenbach test (+): kalo kaki / tangan dimasukkan ke air es pasien mengalami mialgia, shaking chill and voids dark red/
black urine
o Gumma pada palatum , throat, nasal septum.
 Prenatal sifilis: hutchinson teeth, mulberry molar
 Tabes dorsalis: gx klinis parestesi, ataksia, gangguan berkemih, inkontinensia rektum, lightning palms, diminished deep tendon
reflex, poor papillary response to light
 Wassermann test serologis: mengukur antibodi terhadap diphosphatidylcholine atau cardiolipin.
 FTA –ABS: perlu mikroskop fluoeresen
 Pemeriksaan antibodi thd cardiolipin  disebut nontreponemal/nonspesifik. Antibodi terhadap surface-exposed protein:
treponemal/ spesifik test

 IMS 03/05/2017 22:29:00
 Tx HIV:
DHHS guide- lines allow for selection from a variety of preferred regimens. The basic recommendation is to select two
nucleoside reverse transcriptase inhibitors (NRTI), one of which is lamivudine (3TC) or emtricitabine (FTC), plus either an
NNRTI (efavirenz [EFV] is the preferred agent),94–96 or a protease inhibitor that is pharmacologically boosted by low-dose
riton- avir (lopinavir/ritonavir [LPV/r], fosamprenavir/r, or atazanavir/r are the current preferred protease inhibitors)
 Obat2 antivirus: acyclovir and foscarnet: inhibits DNA polymerase virus , foscarnet: analog pirofosfat dan menghambat DNA
polimerase secara nonkompetitif.
 the vaginal fluid of women with BV has increased levels of endotoxin, sialidase and glycosidases, which degrade mucin and
decrease its viscosity
 Bau amis BV saat ditetes KOH 10% karena amine yg diproduksi oleh flora microbial sbg akibat volatilization of aromatic amines
including putrescine, cadaverine, trimethylamine (t.u ini) at alkaline pH
 Cairan vagina BV: memiliki peningkatan kadar endotoxin, sialidase, glikosidase
 Klasifikasi microbicide sesuai mekanisme kerjanya:
1. nonspesifik antimicrobial
2. nonspesific dan spesific attachment/fusion/entry inhibitor
3. intracellular replication inhibitor
4. unspecified mechanism
 Kultur :
 Chancroid : pake gonoccocal agar base/ Mueller Hinton agar base  ditambah L-glutamin dan vancomycin
 Sifilis: kultur ga bs, animal autoinokulasi pada rabbit
 GO: modified Thayer Martin , transport: stuart mediaxv

 Tx epididimitis:
o oral ofloxacin 400 mg twice daily or levofloxacin 500 mg once daily for a 10-day treatment course
 Terapi gonore pada ibu hamil:
o Ceftriaxone 125 mg im SD, or cefixime 400 mg oral SD
o Atau klo alergi cefalosporin: pake spektinomisin 2 g SD im
o Ga boleh pake tetra
o Tambahin azitro 1 g SD, atau eritromisin 7 hari utk C. tracomatis
 Fitz Hugh Curtis syndrome
o Perihepatitis yg muncul setelah/dengan salpingitis, dicurigai karena GO/CT, ada fever nausea, vomiting. High titers of
57kDa Chlamydial hsp
 HSV:
o Entry: perlu glikoprotein gB, gH, gL, gD (hny ada pada alfa herpesviruses kecuali VZV)
o Membran fusion: pake gD  mengaktifkan aktivitas fusogenik gB (membentuk homooligomer), gH dan gL
(membentuk heterodimer stabil)
o HSV berikatan dgn heparan sulfat pada sel melalui gB or gC( yg gC bs berikatan dgn/menginaktifkan C3 component of
complement, hny utk alfa herpesviruses aja )
o Resisten thd ACV: bs krn: TK defisien, TK- altered, or DNA polimerase resisten strains of HSV.
o Tx utk ACV resisten HSV:
 Foscarnet 40 mg/kg iv tiap 8 jam
 Cidofovir : acylic nucleoside phosphonate, phosphorilated only by cellular enzyme  efektif utk HSV strain
dgn TK defisien/altered
 Trifluridine : srg utk oftalmik herpes, potensi antiviral meningkat dgn pengunaan IFN alfa
 Resiquimod dan imiquimod
o Penggunaan ACV saat kehamilan: bs menyebabkan obstruktive uropathy pada newborn sekunder krn kristal ACV
o Pada hamil dgn HSV: kalo ga ada lesi saat persalinan: boleh per vag. Bila ada lesi aktif di cervix/ external genitallia or
prodrome: wajib SC. Kl bs SC sbelum ruptur membran, no risk to baby
o Tx neonatus: asiklovir 3x 10 mg/kg bb . hari iv selama 5-7 hari
o Komplikasi herpes genital:
 CNS: aseptic meningitis  pemeriksaan CSF: leukosit 10-1000 cells/ mm3, glukosa CSF >50% glukosa darah,
 Proktitis plg sering dgn komplikasi hiperestesia/ anestesi perineal, lower back and sacral region
 Transverse mielitis srg tjd pada infeksi herpes genital primer
 Pada kehamilan: bs abortus, prematur, HSV neonatal, kecuali korioamnionitis akut!!!
o Efek samping ACV: headache n nausea. Kalo pake dosis tinggi (8g/hari) pada pasien immunocompromised: e.s
thrombotik microangiopati.
 CT
 Mekanisme hidup CT:
 Initial attachment of infectious particle / elementary body (EB) pada sel host  membelah tiap 8-18/24 jam
 Entry into sel
 Perubahan morfologi menjadi partikel retikulat, dgn pertumbuhan dan replikasi intraselular
 Perubahan morfologi dari RB menjadi EB,
 Release of infectious particles
 o CT: Serovar A,B,C : trachoma ocular infections, Serovar D-K: ocular, genital dan respiratory infections  A-K hanya
terbatas pada mukosa (A konjungtivitis, B-C pneumonia, D-K :uretritis klamidia  terdeteksi 7-14 hari setelah infeksi
o Bs terjadi anterior uveitis ok CT
o Reiter’s syndrome : infeksi oleh CT dgn trias arthritis, uretritis, konjungtivitis (uveitis), Tjd pada individu dgn HLA B27
o Keratoderma blenorhagicum: dull red papul yg dgn cepat membentuk permukaan hiperkeratotik kekuningan  pd px
HIV menyerupai postular psoriasis
o Terapi CT pada anak2:
 Older children: eritromisin 50 mg/kg/hari 4x sehari p.o max 2 g/hari selama 7-14 hari
 Anak>8 tahun: tetrasiklin 25-50mg/kg/hari 4x sehari p.o selama 7 hari
 Azitromisin 1 g p.o SD  untuk anak2 ≥ 45 kg dan/atau ≥ 8 tahun

 GO:
o Ligand utk adhesi: pili, Opa, Porin dan LOS
o Pili: membuat GO menempel lebih baik ke sel kolumnar dibanding skuamous sel
o Infeksi GO pada wanita tidak bs terjadi di vagina of sexually mature women: krn epitelnya tidak mensupport growth of
N. gonore lokasi infeksi lain selain endocervix: bartolin dan Skene glands, uterus, Falopian tubes, ovarium, PID,
uretritis
o Disseminated GO infection: acute arthritis dermatitis syndrome  tdd triad dermatitis ( small to medium macules or
hemoragic vesicopustul on an erythematous base located on palms and soles or trunk and extremieties ( gun metal
gray)), migratory polyarthritis (bs pada single joint atau multiple joint asimetris,biasanya monoarticular atau
pauciarticular), dan tenosynovitis.
o Terapi GO dan suseptibilitas:
 Penicillin : accumulation of several chromosomal mutations that affect cell surface structure :
 penA,alteration of penicilin binding protein 2 (PBP2), shg afinitas PBP2 utk penisilin menurun
 mtr  encode represor mtrCDE efflux pump  reduce intracellular concentrations of antibiotics
 penB involve point mutations of porB entry of antibiotic through porin channel is altered
 Tetracycline : ada mutasi kromosom atau adanya plasmid TCr
 Spectinomycin : alter ribosomal target utk Spectinomycin
 Streptomycin : resistance to Str maps near spc
o Trigonitis: Poliuria, disuria terminal dan hematuria~!!!
o Tes oksidasi: untuk menentukan identifikasi bakteri
 HIV:
o Perlekatan HIV pada sel host dimulai dgn membentuk ko-reseptor CCR5 ( bs infect both macrofag dan CD4 T cell), tp
bs jg membentuk koreseptor CXCR4 ( hny menginfeksi CD4 T cells) berhub dgn more rapid disease progression
o T tropik: difasilitasi oleh CXCR4, menginfeksi sel T CD4,
o M tropik : difasilitasi oleh CCR5, menginfeksi makrofag
 HPV:
o HPV 16: pny oncoprotein E6 memiliki afinitas kuat dan dapat merusak p53
 H. ducreyi:
o Membutuhkan hemin dalam pertumbuhannya: uji porfirin!!
o Tumbuh dalam : gonococcal agar base, 2% bovine hemoglobin, 5% fetal calf serum, Mueller Hinton
 Penyebab uretritis persisten:
o Tricomonas vaginalis: cari di uretra anterior, semen, prostat dan epididimis
 LGV:
 LGV (Nicolas Favre disease): serovar L1-L3, dimana yg paling sering L2b  L1-L3 lbh invasiv dan high affinity for
macrofag jd inokulasi di permukaan mukosa replikasi di dalam makrofag ke Limfnode jadi limfadenitis
 Buchblatt condyloma: pada sindroma genital/ estiomene, permukaan elefantiasis labia dapat terjadi tumor polipoid dan
verukosa yg kadang berbentuk pipih
 Greenblatt sign: sign of groove
 Ada stalate abses triangular/ quadrangular
 Sindroma anogenitorectal: proktokolitis, hiperplasia intestinal & jar limfatik perirektal
 Pemeriksaan:
o Frei test  dari pus unruptured buboes, dilusi dalam salin dan sterilized by heating, kultur LGV pada yolk sac
dari embrio ayam. Frei test (+) setelah bubo muncul 2-8 minggu setelah infeksi
o Complement fixation test (+) bila nilai titer 1:64
o PCR/ NAAT
o microIF antibody test
o rectal stricture caused by LGV cek by barium enema: beda dgn Ca: lebih panjang, sedikit perubahan pada
permukaan mukosa bowel, tendency to form fistula yg reenter lumen of rectum.
 Trikomoniasis:
 Tx metro/ tinidazole 2 g po SD or alternatif: metro 2x 500 mg selama 7 hari
 Klo gagal dan tidak terbukti ada reinfeksi: metro 2 g 1x1 selama 3-5 hari
 Metro gel: gak ngefek utk trikomonas
 Donovanosis:
 Penyebab: Calymmatobacterium granulomatis
  Perlu low redox potential  pake medium thioglikolat, dan perlu faktor2 dalam telur  ganti pake enzim bovine
albumin / soya meal
 IMS pubertas : cek chlamydia dan GO
 Laktobasilus: urutan jenis terbanyak
o L. crispatus, L. gasseri, L. jensenii, L. vaginalis dan L. iners (Cowo Ganjen Jualan Volvo Indonesia)
 Ulkus sifilis yang ditemukan pada skabies: chancre galeuse
 KVV pada HIV: ketoconazole 100 mg per hari selama 6 bulan
o Pada sekret vagina dgn KVV: ada enzim aspartyl proteinase yg dihasilkan oleh candida
 Epitel vagina pre menarch: tipis dan fragile, little glikogen/ glucose dalam vaginal fluid. Pada saat pubertas: epitel vagina
menebal ec estrogen, glikogen>>>  dimetabolisasi oleh sel epitel mnjd glukose lactic acid  membuat pH cairan vagina
asam dari pH 7 (pada prepubertas) menjadi 5