DD Vaginal Discharge
DD Ulkus genital
Gonorrhea → bagian dari sindrom duh
Microbiologi
1. Gram(-) , intraseluler, aerobic & anaerob, diplococcus
2. Columntar / cuboidal epithelium → semua membran mukus,
3. Entry = pinocytosis
4. Pili = nempel ke mukosa, resistensi thdp WBC, bergerak secara retrograde ke
saluran reproduksi atas
5. Opacity-associated (Opa) protein = penempelan ke WBC, invasi ke sel host,
menurunkan sistem imun
6. PorA, PorB = meningkatkan invasi ke epitel → meningkatkan risiko
bacteremia
Patofisiologi
1. Men most common = Anterior urethra
2. Women most common = Endocervix (80%-90%), urethra (80%), rectum (40%),
and pharynx (10%-20%)
3. Localized & Disseminated (DGI) Gonococcemia
Faktor risiko
Komplikasi
Faktor risiko
Pria → Tertular oleh pasangan seksual, Menderita DM, Tidak disirkumsisi
Wanita → lingkungan hangat & lembab, kontrasepsi hormonal & spiral,
antibiotik broad-spectrum, DM, imunokompromais, hamil, douching
Patofisiologi
1. Women = vagina, cervix, urethra, bladder, and Bartholin and Skene glands
2. Men = anterior urethra, external genitalia, prostate, epididymis, and semen
3. Destroys epithelial cells by direct cell contact & release of cytotoxic substances
4. Binds to host plasma proteins = preventing recognition of the parasite by the
alternative complement pathway and host proteinases
Faktor risiko
Gambaran klinis
Tatalaksana
Komplikasi
Patofisiologi
1. Altered vaginal flora = known and unknown mechanisms → increase in
the local pH
2. May result from a reduction in the H2O2–producing lactobacilli (protective factors
= maintain the acidic pH of healthy vaginas and inhibit other anaerobic
microorganisms through elaboration of hydrogen peroxide)
3. In BV, the lactobacilli population is reduced greatly, while populations of various
anaerobes and G vaginalis are increased.
4. G vaginalis forms a biofilm in the vagina → resistant to some forms of
medical treatment survive in H2O2, lactic acid, and high levels of
antibiotics.
Faktor risiko
- Smoke
- Sexually active
- Douche
- Recent antibiotic use
- Decreased estrogen production
- Wearing IUD
Gambaran klinis
1. half of the time, asymptomatic
2. Burning feeling when you pee
3. Fishy smell that gets stronger after sex
4. Itching
5. Thin white, gray, or green discharge
6. It's not the same as a yeast infection. Those often have a thick white discharge
that doesn’t smell.
2. Pemeriksaan Mikroskopik
- Clue cells on a saline smear = vaginal epithelial cells that have bacteria
adherent to their surfaces.
- The edges of the squamous epithelial cells, which normally have a
sharply defined cell border, become studded with bacteria.
- The epithelial cells appear to be peppered with coccobacilli
4. Vaginal cultures
Tatalaksana
1. Metronidazol 2 x 500 mg selama 7 hari,
2. Metronidazol 2 gram
3. Klindamisin 2 x 300 mg PO selama 7 hari
4. Tinidazol 2 x 500 mg selama 5 hari,
5. Ampisilin atau amoksisiin dengan dosis 4 x 500 mg per oral selama 5 hari
Komplikasi
1. Most cases = no complications
2. BV increase a woman's susceptibility to HIV infection
3. Increases the chances that an HIV-infected woman can pass HIV to her sex
partner.
4. Increase in the development of an infection following surgical procedures such
as a hysterectomy or an abortion.
5. Pregnant = increased risk for some complications of pregnancy (preterm
delivery)
6. Increase a woman's susceptibility to other STDs, such as herpes simplex virus
(HSV), chlamydia and gonorrhea.
Sifilis / Lues veneria / lues / raja singa
Microbiologi
Patofisiologi
Gambaran klinis
SIFILIS I
SIFILIS II
SIFILIS III
1. Bentuk lesi khas guma = infiltrat sirkumskrip kronis, lunak & destruktif, besar
lentikuler bisa sampai sebesar telur ayam
2. Awal lesi ≠ tanda radang akut & dapat digerakkan, beberapa bulan
jadi lunak dari tengah & tanda radang mulai tampak
3. Perforasi & keluar cairan seropurulent, kadang sanguinolen / jaringan nekrotik
4. Tempat perforasi menjadi ulkus
5. Dapat soliter / multiple
6. Tulang = tibia, tengkorak, bahu, femur, fibula, humerus
7. Organ = hepar, esophagus, lambung, paru, ginjal, VU, prostat, KV, CNS
Bentul lesi
Pemeriksaan penunjang
Pemeriksaan T.pallidum → Diambil dari mengambil serum dari lesi kulit dan
dilihat bentuk dan pergerakannya dengan mikroskop lapangan gelap.
Dilakukan 3 hari berturut
1. Penisilin G benzatin → 7,2 jt unit, IM 2,4 juta unit sekali suntik (3kali), 1
kali seminggu
HIV tanpa komplikasi
Microbiologi
HIV - Human Immunodeficiency Virus
Patofisiologi
Faktor risiko
Gambaran klinis
Terdapat 3 tingkatan
1. tingkat 1
a. tanpa gejala sama sekali
b. LGP
2. tingkat 2
a. penurunan BB kurang dari 10%
b. kelianna mulut dan kulit yang ringan, misalnnya dermatitis, seboroik,
prurigo, onikomikoisis, ulkus pada mulut yang berulang dna keilitis
angularis
c. ISPA berulang, misal sinusitis
3. Tingkat 3
a. penurunan BB lebih dari 10%
b. diare kronik > 1 bulan, tanpa sebab
c. demam tidak diketahui penyebab > 1 bulan, hilang timbul
d. kandidosis mulut
e. bercak putih berambut di mulut (hairy leukoplakia)
f. TB paru setahun terakhir
g. infeksi bakteri berat, misal pneumonia
4. tingkat IV
a. Sarkoma koposi pada laki-laki dibawah 60 tahun
b. limfoma (non-Hodgkin)
c. karsinoma sel skuamosa pada mulut dan anus
Gambaran klinis
1. Asymptomatic
2. Umumnya tidak ada gejala sistemik
3. Lesi kulit
a. Medscpae → nontender, single/multiple, rounded, dome-shaped,
flesh-colored, waxy papules 2-5 mm (giant molluscum = 1,5 cm)
in diameter; papules umbilicated & contain caseous plug
b. FK UI → bentuk papul bulat mirip kubah, berukuran miliar -
lentikular berwana putih dan berkilat seperti lilin. papul
membesar lama2 menjadi delle (ada lekukan di tengah)
1. typically = chest, arms, trunk, legs, and face; palms are spared
2. 10% develop eczema
Tatalaksana
1. Self-limited = 6-9 months; some 3-4 years
2. Individual lesion seldom persist >2mo
3. repeat examination 2-4wk after treatment → retreatment
4. Direct lesional trauma = Cryotherapy, lasers, curettage
5. Immune response stimulation
6. Antiviral therapy
7. Anak
a. Kantaridin 0,7-0,9%
b. kantaridin - salisilat
i. untuk kantradin → dioleskan lalu didiamkan 4 jam→ dicuci
c. imiquimod 1-5%
d. anti nyeri → asetaminofen
e. bila gelembung pecah → oles Natrium fusidat / mupirosin
Komplikasi
1. Bacterial superinfection, irritation, inflammation
a. Staphylococcus aureus = abscess formation
b. Pseudomonas aeruginosa = necrotizing cellulitis
Herpes simpleks = Herpes genital
Definisi
Infeksi akut yang disebabkan oleh virus herpes simpleks (virus herpes hominis) tipe I
atau tipe II yang ditandai oleh adanya vesikel yang berkelompok di atas kulit yang
sembab dan eritematosa pada daerah dekat mukokutan, sedangkan infeksi dapat
berlangsung baik primer maupun rekurens
Transmisi
Kontak langsung (kulit-kulit, kulit-mukosa, mukosa-mukosa)
Patogenesis
1. Transmisi terjadi via inokulasi pd permukaan mukosa yang rentan/mikrolesi pd
kulit
2. Stlh paparan thd HSV, virus replikasi pd sel epitel → lisis sel yg
terinfeksi → pembentukan vesikel → inflamasi lokal
3. Setelah infeksi primer, HSV naik melalui saraf sensorik perifer menuju ganglia
saraf sensorik/autonomik
4. Dapat berpindah secara retrograde, menginfeksi neuron tanpa simptom
Infeksi Primer
● Tempat predileksi VHS tipe I → daerah pinggang ke atas terutama di
daerah mulut & hidung
○ Anak → inokulasi dpt tjd scr kebetulan, misalnya kontak kulit pd
perawat, dokter gigi, atau pd org yg sering menggigit jari
(herpetic whit-low)
○ Juga sebagai penyebab herpes ensefalitis
● Tempat predileksi VHS tipe II → daerah pinggang ke bawah, terutama
derah genital, juga dpt menyebabkan herpes meningitis & infeksi
neonates
● Infeksi primer berlsg >lama & >berat (±3 mgg) & sering disertai gejala sistemik
(demam, malaise, anoreksia, pembengkakan KGB regional)
● Kelainan klinis yg dijumpai : diawali dengan LENTING
○ Vesikel berkelompok di atas kulit yg sembab & eritematosa, berisis cairan
jernih & kemudian menjadi seropurulen, dpt menjadi krusta & kdg alami
ulserasi yg dangkal, biasanya sembuh tanpa sikatriks
○ Perabaan tdk ada indurasi
Fase Laten
1. Pada penderita tidak ditemukan gejala klinis
2. VHS dapat ditemukan dalam keadaan tidak aktif pada ganglion dorsalis
Infeksi Rekuren
1. VHS pada ganglion dorsalis tidak aktif → dengan mekanisme pacu
menjadi aktif & mencapai kulit → menimbulkan gejala klinis
2. Mekanisme pacu dpt berupa : trauma fisik (demam, infeksi, kurang tidur, hub
seks, dsb), trauma psikis (gangguan emosional, menstruasi), dapat timbul
karena jenis makanan & minuman yg merangsang
3. Gejala klinis yg timbul >ringan drpd infeksi primer, berlangsung kira2 7-10 hari
4. Sering ditemukan gejala prodromal lokal sblm timbul vesikel berupa rasa panas,
gatal, nyeri
5. Infeksi rekurens dpt timbul pd tempat yg sama (loco) atau tempat lain/ tempat di
sekitarnya (non loco)
Pemeriksaan Lab
1. Riwayat dan temuan klinis
2. Pasien dgn lesi: kultur + dlm 48-96 jam setelah inokulasi
a. Kultur saat vesicular stage, dari pasien immunocompromised,
infeksi primer → most successful culture
3. PCR lebih sensitif dibanding isolasi virus, berguna untuk deteksi HSV saat late-
stage ulcerative lesion
4. Tzank smear
Pengobatan
Imunokompeten UTAMA DI UT
1. First episode →
a. Asiklovin 5x200/hari PO selama 7 hari, ATAU
b. Asiklovir 3 x 400 mg/hari PO selama 7 hari, ATAU
c. Valasiklovir 2 x 500 mg/hari PO selama 7 hari
2. Symptomatic recurrent genital herpes
a. Asiklovin 5x200/hari PO selama 5 hari, ATAU
b. Asiklovir 3 x 400 mg/hari PO selama 5 hari, ATAU
c. Valasiklovir 2 x 500 mg/hari PO selama 5 hari
Immunosupressed
1. Acute symptomatic first or recurrent episodes → IV acyclovir
(5 mg/kg q8h) or oral acyclovir (400 mg qid), famciclovir (500 mg
bid or tid), or valacyclovir (500 mg bid), vary from 7 to 14 days. IV therapy may
be given for 2–7 days until clinical improvement and followed by oral therapy.
Suppression of reactivation disease (genital or oral–labial) → asiklovir 2 x
200 hingga 4 x 200 mg 6 bulan
Skabies
Parasitologi
1. Menyerang epidermis → Stratum corneum → hanya betina
2. 4 pasang kaki (2 depan, 2 belakang)
a. Kaki 1 & 2 = ambulakra
b. Jantan kaki 3 bulu cambuk, kaki 4 ambulakra
c. Betina kaki 3 & 4 ambulakra
Penularan
1. Direct skin-to-skin contact or indirect contact
Patofisiologi
1. telur inkubasi dan menetas dalam 3-4 hari
2. Larva migrasi ke permukaan kulit dan menggali ke dalam stratum korneum
3. Mating → jantan langsung mati, betina fertil seumur hidup dan bertelur
4. Betina membuat terowongan dengan enzim proteolitik dan melarutkan stratum
corneum sekaligus melepaskan telur
5. Betina hidup selama 1-2 bulan
Faktor risiko
1. tinggal dekat dengan pasien carrier skabies
Gambaran klinis
1. Lesi kulit
a. Pathognomonic = Burrows → berwarna putih/keabuan berbentuk
garis atau lurus.
b. lesi kulit menyerupai dermatitis, dengan adanya papul, vesikel,
urtika bila digaruk → timbul erosi, ekskoriasi, krusta
2. Gejala Klinis
1. Pruritus nokturna
Patofisiologi
1. Large claws = grasp the coarser pubic hairs in the groin, perianal, and axillary
areas
2. Crawl up to 10 cm/day.
3. cannot survive off the human host for >1 day
4. Heavy infestation = involve eyelashes, eyebrows, facial hair, periphery of the
scalp
Faktor risiko
Gambaran klinis
1. Pruritus
2. Pathognomonic = maculae cerulea (bluish-gray macules) = karena digigit
3. Crusts and pinpoint blood staining (Black dot) may also be noted on underwear
Komplikasi
Adenitis inguinal, ulkus chancroid, fimosis atau parafimosis, fisura uretra, fistel
rektovagina
Kondiloma akuminata = HPV
Microbiology & Etiology
1. 90% = HPV types 6 and 11 = least likely to have a neoplastic potential, moderate
neoplastic potential (types 33, 35, 39, 40, 43, 45, 51-56, 58) or high neoplastic
potential (types 16, 18)
Pathophysiology
1. Cells of the basal layer of the epidermis are invaded by HPV
2. Penetrate through skin → mucosal microabrasions.
3. A latent viral phase begins with no signs or symptoms and can last from a month
to several years.
4. Following latency, production of viral DNA, capsids, and particles begins. Host
cells become infected and develop the morphologic atypical koilocytosis of
condyloma acuminatum.
5. Most commonly affected areas are the penis, vulva, vagina, cervix, perineum,
and perianal area.
6. Uncommon mucosal lesions in the oropharynx, larynx, and trachea.
7. HPV-6 even has been reported in other uncommon areas
8. Infection by direct manual contact or indirectly by fomites rarely may occur
Risk Factors
1. Smoking, oral contraceptives, multiple sexual partners, and early coital age
Clinical Presentation
1. Single or multiple papular eruptions. Eruptions may appear pearly, filiform,
fungating, cauliflower, or plaquelike.
2. can be quite smooth (particularly on penile shaft), verrucous, or lobulated.
3. Eruptions may seem harmless or may have a disturbing appearance.
4. Eruptions' color may be the same as the skin, or they may exhibit erythema or
hyperpigmentation.
5. Check irregularity in shape, form, or color suggestive of melanoma or
malignancy.
6. The chief complaint usually is one of painless bumps, pruritus, or discharge.
7. Involvement of more than 1 area is common. History of multiple lesions, rather
than 1 isolated wart, is common
8. Search for evidence of other STDs
Testing
1. Acetowhitening: Subclinical lesions can be visualized by wrapping penis with
gauze soaked with 5% acetic acid for 5 minutes. Using a 10-X hand lens or
colposcope, warts appear as tiny white papules. A shiny white appearance of
skin represents foci of epithelial hyperplasia (subclinical infection)
2. Filter hybridization (Southern blot and slot blot hybridization), in situ hybridization,
and PCR: diagnosis and HPV typing
Treatment
- Cryotherapy
- Electrodesiccation
- Curettage
- Surgical excision
- Carbon dioxide laser treatment
- TCA 80-90% di totol dan harus diulang
- Podofilin 25% di oles, dicuci setelah 4-6 jam, diulangi setelah 3 hari
Prognosis