PENUNTUN PRAKTIKUM

PATOLOGI ANATOMI
SEMESTER GENAP
TA. 2022-2023

BAGIAN PATOLOGI ANATOMI

PROGRAM STUDI
PENDIDIKAN DOKTER
FAKULTAS KEDOKTERAN
UNIVERSITAS MUHAMMADIYAH
SUMATERA UTARA
TAHUN 2023
Penyusun:
Dr. dr. Humairah M. Liza Lubis, M.Ked.(PA), Sp.PA
Dr. Siti Mirhalina Hasibuan, Sp.PA
dr. Ren Astrid A. Siregar, M.Ked.(PA), Sp.PA
dr. Rita Juliana Pohan, M.Ked.(PA), Sp.PA

Penyunting:
Prodi Pendidikan Dokter

BAGIAN PATOLOGI ANATOMI

PROGRAM STUDI PENDIDIKAN DOKTER
FAKULTAS KEDOKTERAN UNIVERSITAS
MUHAMMADIYAH SUMATERA UTARA
TAHUN 2023
 KATA PENGANTAR

Assalamualaikum Warahmatullahi Wabarakatuh.

Alhamdulillah, segala puji dan syukur kehadirat

Allah SWT atas berkat limpahan rahmat dan karunia-
Nya sehingga Buku Penuntun Praktikum Patologi
Anatomi Fakultas Kedokteran Universitas
Muhammadiyah Sumatera Utara tahun 2023 telah dapat
diselesaikan. Buku penuntun ini adalah suatu
penyempurnaan dari buku sebelumnya, yang dapat
membantu para mahasiswa dalam mempelajari konsep-
konsep kelainan penyakit serta mempermudah
mempelajari materi penyakit terutama ditinjau dari
gambaran makroskopis dan mikroskopis yang
sebelumnya telah didapatkan pada mata kuliah didalam
kelas, serta memberikan petunjuk praktis agar
mahasiswa mendapatkan gambaran dengan secara jelas
dalam penyelesaian tugas praktikum.
Kami sampaikan terimakasih kepada Dekan,
Wakil Dekan I dan Wakil Dekan III serta para ketua dan
sekretaris program studi. Terimakasih juga kami
sampaikan kepada Prof. dr. H.M. Nadjib Dahlan Lubis,
Sp.PA(K) atas segala kontribusi didalam
penyempurnaan buku ini.

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 Kami menyadari masih terdapat banyak
kekurangan dalam buku ini. Untuk itu kritik dan saran
yang membangun demi penyempurnaan buku ini sangat
diharapkan. Dan semoga buku ini dapat memberikan
maanfaat bagi mahasiswa FK UMSU khususnya dan
bagi semua pihak dari segala lapisan yang
membutuhkan.

Medan, Juni 2023

Kepala Bagian Patologi Anatomi

Dr. dr. Humairah M. Liza Lubis, M.Ked.(PA)., Sp.PA

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 DAFTAR ISI

KATA PENGANTAR ................................................ 1

DAFTAR ISI............................................................... 3
VISI, MISI DAN TUJUAN......................................... 5
PERATURAN PRAKTIKUM .................................... 7
SISTEM PENILAIAN PRAKTIKUM ...................... 10

PATOGENESIS NEOPLASMA PADA SISTEM

REPRODUKSI WANITA......................................... 11
1. Tujuan Praktikum ............................................ 11
2. Landasan Teori................................................ 11
2.1. Kista Bartholin ......................................... 11
2.2. Condylomata Acuminata .......................... 13
2.3. Servisitis .................................................. 15
2.4. Polyp ........................................................ 16
2.5. Kista Nabothian ........................................ 17
2.6. Endomteriosis........................................... 18
2.7. Leiomioma Uteri ...................................... 19
2.8. Serous Cystadenoma Uteri ........................ 20
2.9. Mucinous Cystadenoma Uteri ................... 21
2.10. Dysgerminoma ....................................... 22
2 11. Mature Cystic Teratoma (Dermoid Cyst) 23
3. Prosedur Praktikum ........................................... 24
3.1. Alat dan bahan ......................................... 24
3.2. Cara kerja ................................................. 24
3.3. Hasil praktikum ........................................ 24
DAFTAR PUSTAKA ............................................... 26
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PATOGENESIS NEOPLASMA PADA PAYUDARA
.................................................................................. 27
1. Tujuan Praktikum ............................................ 27
2. Landasan Teori................................................ 27
2.1. Fibroadenoma Mammae ........................... 27
2.2. Karsinoma Mammae ................................ 29
3. Prosedur Praktikum ........................................... 32
3.1. Alat dan bahan ......................................... 32
3.2. Cara kerja ................................................. 32
3.3. Hasil praktikum ........................................ 33
DAFTAR PUSTAKA ............................................... 34

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 Visi, Misi dan Tujuan
Prodi Pendidikan Dokter FK UMSU

Visi
Menjadi pusat unggulan bagi pendidikan kedokteran
dalam pengembangan ilmu pengetahuan dan sumber
daya manusia yang profesional dan berorientasi
komunitas berdasarkan nilai-nilai al-Islam dan
kemuhammadiyahan di Indonesia pada tahun 2030.

Misi
1. Menyelenggarakan pendidikan dan pengajaran
ilmu kedokteran yang berbasis kompetensi dan
berdasarkan nilai-nilai Islam dan
kemuhammadiyahan.
2. Menyelenggarakan penelitian dan pengembangan
ilmu pengetahuan di bidang ilmu kedokteran
berdasarkan nilai-nilai Islam dan
kemuhammadiyahan.
3. Menyelenggarakan pengabdian kepada
masyarakat berkelanjutan di bidang ilmu
kedokteran berdasarkan nilai-nilai Islam dan
kemuhammadiyahan.
Tujuan
1. Membentuk mahasiswa yang cerdas, kreatif,
inovatif, beretika dan memiliki kemampuan
belajar mandiri dan belajar sepanjang hayat.

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2. Menghasilkan lulusan yang profesional,
kompeten, berdedikasi, berwawasan islami sesuai
dengan Standar Kompetensi Dokter Indonesia
(SKDI) dan Standar Kompetensi dan
Karakteristik Dokter Muhammadiyah (SKKDM).
3. Meningkatkan jumah penelitian berbasis hibah
dan kompetisi.
4. Meningkatkan jumlah publikasi ilmiah di jurnal
nasional dan internasional yang bereputasi.
5. Meningkatkan jumlah pengabdian kepada
masyarakat untuk mewujudkan masyarakat yang
sehat dan berpengetahuan.
6. Mewujudkan tata kelola yang transparan dan
akuntabel.
7. Meningkatkan kinerja dosen dan pegawai.
8. Meningkatkan kualitas sumber daya manusia.
9. Meningkatkan kuantitas dan kualitas sarana dan
prasarana penunjang kegiatan akademik.
10. Membangun atmosfer akademik.

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 PERATURAN PRAKTIKUM

Tahapan kegiatan praktikum:

1. Mahasiswa mengikuti pre test di elearning sesuai
jadwal yang sudah ditentukan. Mahasiswa yang
tidak mengikuti pre test akan mempengaruhi nilai
akhir praktikum.
2. Mahasiswa mengikuti seluruh praktikum secara
online via zoom meeting sesuai jadwal yang sudah
ditentukan. Mahasiswa yang tidak hadir dengan
alasan sesuai panduan akademik yang dibenarkan
dapat mengikuti inhal/susulan praktikum.
3. Mahasiswa mengerjakan tugas/laporan
penyusunan praktikum dan mengumpulkannya
sesuai ketentuan masing-masing bagian
laboratorium terkait.
4. Mahasiswa mengikuti post test sesuai jadwal blok
yang sudah ditentukan. Prasyarat ikut ujian post
test adalah mahasiswa mengikuti seluruh
praktikum (online). Jika mahasiswa tidak hadir
post test dengan alasan sesuai dengan panduan
akademik maka mahasiswa dapat mengikuti post
test susulan (Inhal).

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Tata tertib praktikum daring/online:
1. Mahasiswa wajib mengunduh bahan ajar/video
praktikum di elearning FK UMSU dan belajar
mandiri untuk persiapan kegiatan praktikum.
2. Mahasiswa wajib hadir minimal 10 menit
sebelum kegiatan dimulai pada zoom meetingatau
pada laboratorium. Mahasiswa yang terlambat
lebih dari 10 menit tidak diperkenankanmengikuti
kegiatan praktikum.
3. Pada praktikum online (zoom meeting):
- Mahasiswa wajib mengaktifkan kamera
(terlihat jelas seluruh wajah) dan tidak
melakukan aktifitas lain saat kegiatan
berlangsung, seperti berkendara, makan dan
lain-lain.
- Mahasiswa wajib mengenakan busana yang
sopan dan sesuai dengan peraturan busana
kegiatan praktikum Fakultas Kedokteran
UMSU
- Mahasiswa wajib mempersiapkan perangkat
dan jaringan internet sebelum mengikuti
kegiatan praktikum. Mahasiswa yang keluar
zoom karena masalah jaringan, maka wajib
segera masuk kembali ke link zoom dan
melapor kepada petugas laboran laboratorium
(Sdri. Kiki Anisa, No HP 082168614741),dan
petugas laboran laboratorium wajib
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 mencatat di berita acara praktikum di hari
yang sama praktikum berlangsung.
- Kehadiran mahasiswa dihitung berdasarkan
durasi mengikuti kegiatan praktikum zoom
meeting. Durasi kehadiran mahasiswa yang
kurang dari 75 menit dianggap tidak hadir.
4. Mahasiswa yang tidak hadir karena alasan yang
dapat dibenarkan sesuai panduan akademik dapat
mengikuti kegiatan susulan (inhal) sesuai dengan
peraturan yang berlaku.
5. Mahasiswa yang tidak mengikuti kegiatan
praktikum secara lengkap tidak diperkenankan
untuk ujian praktikum (post test) dan selanjutnya
tidak memenuhi syarat untuk mengikuti ujian
blok.

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 SISTEM PENILAIAN PRAKTIKUM

Penilaian praktikum dibagi berdasarkan nilai:

1. Pre test (20%)
2. Tugas (20%)
3. Post Test (50%)
4. Attitude (10%)

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 PATOGENESIS NEOPLASMA PADA SISTEM
REPRODUKSI WANITA

1. Tujuan Praktikum
Tujuan Umum: Mahasiswa mengetahui gambaran
makroskopis dan mikroskopis dari lesi infeksi dan
neoplasma yang dijumpai pada sistem reproduksi
wanita.

Tujuan Khusus:
1. Mahasiswa mengetahui gambaran makroskopis dan
mikroskopis lesi dari vulva.
2. Mahasiswa mengetahui gambaran makroskopis dan
mikroskopis lesi dari serviks.
3. Mahasiswa mengetahui gambaran makroskopis dan
mikroskopis lesi dari endometrium.
4. Mahasiswa mengetahui gambaran makroskopis dan
mikroskopis lesi dari ovarium
2. Landasan Teori
2.1. Kista Bartholin
Kista adalah kantung yang berisi cairan atau bahan
semisolid yang terbentuk di bawah kulit atau di suatu
tempat di dalam tubuh. Kista bartholin terjadi akibat
oklusi peradangan duktus utama kelenjar bartholin
vulvovaginal. Kista bartholin terjadi akibat oklusi
peradangan duktus utama kelenjar bartholin
vulvovaginal. Obstruksi peradangan ini dapat
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 disebabkan oleh gonore dan infeksi lain, peradangan
atau iritasi jangka panjang. Apabila saluran kelenjar ini
mengalami infeksi maka saluran kelenjar ini akan
melekat satu sama lain dan menyebabkan timbulnya
sumbatan. Cairan yang dihasilkan oleh kelenjar ini
kemudian terakumulasi, menyebabkan kelenjar
membengkak dan membentuk suatu kista. Suatu abses
terjadi bila kista menjadi terinfeksi dan harus didrainase.
Kelenjar bartholin dibentuk oleh kelenjar
racemose dibatasi oleh epitel kolumnar atau kuboid.
Duktus dari kelenjar bartholin merupakan epitel
transisional yang secara embriologi merupakan daerah
transisi antara traktus urinarius dengan traktus genital.
Kista tanpa peradangan dilapisi oleh epitel
transisional atau epitel gepeng.

Gambar 1. Makroskopis menunjukkan kista unilocular berukuran 5,5 x 4 x 3

cm yang berisi cairan serous dan dinding bagian dalam halus berkilau.
Sumber referensi: https://www.webpathology.com

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Gambar 2. Mikroskopis menunjukkan lapisan epitel transisional dan kelenjar
mucous. Pelapis kista sebagian atau keseluruhan dapat rusak oleh infiltrasi
sel-sel inflamasi.
Sumber referensi: https://www.webpathology.com

2.2. Condylomata Acuminata

Lesi verukosa seperti kutil tumbuh di vulva,
perineum, vagina, dan pada serviks (jarang). Lesi ini
ditularkan melalui hubungan seksual dan ditimbulkan
oleh human papilloma virus (HPV) terutama tipe 6 dan
11. Histologik, terdiri atas proliferasi epitel skuamosa
berlapis seperti pohon dengan vakuolisasi perinuklear
yang khas pada sel skuamosa, disebut koilositosis,
karena efek virus. Lesi ini jinak, tetapi sering multiple
dan bersamaan dengan fokus-fokus displasia atau
bahkan karsinoma.

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 Gambar 3. Makroskopis Condilomata acuminata yang disebabkan oleh
human papilloma virus bermanifestasi sebagai kutil dan nodul pada genital.
Sumber referensi: Kumar V, Abbas AK, Fousto N, Aster. Pathologic Basis of
Disease. Tenth Edition. Elsevier Saunders. 2017

Gambar 4. Mikroskopis Condilomata acuminata terlihat proliferasi sel epitel

skuamosa dengan vakuolisasi perinuklear (koilositosis).
Sumber referensi: Kumar V, Abbas AK, Fousto N, Aster. Pathologic Basis of
Disease. Tenth Edition. Elsevier Saunders. 2017

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2.3. Servisitis
Dapat disebabkan oleh infeksi spesifik seperti
gonokokus, Trichomonas vaginalis, candida dan
micoplasma atau oleh bakteri aerob dan anaerob
endogen vagina seperti streptokokus, enterokokus, E.
coli dan stafilokokus (servisitis nonspesifik).
Servisitis akut yang paling sering ditemukan pasca
partus dan ditandai oleh infiltrasi akut neutrofil di bawah
garis mukosa.
Servisitis kronik jauh lebih sering dan walaupun
dapat disebabkan oleh salah satu patogen yang telah
disebut sebelumnya, sering tidak diketahui etiologinya.
Peradangan dapat mengakibatkan stenosis duktus
kelenjar serviks dan terbentuk kista nabothian yang
dilapisi oleh epitel kolumnar. Juga dapat ditemukan
metaplasia skuamosa kelenjar endoserviks.
Servisitis kronik adalah jinak, tetapi atipia reaktif
harus dibedakan dari displasia serviks.

Gambar 5. Makroskopis servisitis mukourulen yang disebabkan oleh

clamidia menunjukkan ektopi, edema dan discharge.
Sumber referensi: Kumar V, Abbas AK, Fousto N, Aster. Pathologic Basis of
Disease. Tenth Edition. Elsevier Saunders. 2017
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 Gambar 6. Atas: Pada diagram, reserve cells pada zona transformasi
bergabung dengan sel-sel basal ektoserviks (kanan) dan dapat berlanjut
menjadi diferensiasi kolumnar dan skuamosa(metaplasia) Bawah: (dari kiri
ke kanan). Perubahan sel epitel serviks berupa diferensiasi kolumnar (kedua
dari kiri), metaplasia skuamosa (kedua dari kanan) dan epitel skuamosa
ektoserviks (kanan).
Sumber referensi: Kumar V, Abbas AK, Fousto N, Aster. Pathologic Basis of
Disease. Tenth Edition. Elsevier Saunders. 2017

2.4. Polyp
Polyp endoserviks merupakan tumor jinak dan
terdiri stroma jaringan ikat yang mengandung kelenjar-
kelenjar berdilatasi dan dilapisi oleh epitel endoserviks.

Gambar 7. Mikroskopis polip dikarakteristikkan dengan pertumbuhan

berlebih stroma yang dilapisi oleh epitel benign. Pada polip endoservikal
dilapisi oleh epitel skuamokolumnar atau metaplastik skuamosa
sedangkan ektoservikal dilapisi oleh skuamosa berlapis. Stroma
mengandung pembuluh darah berdinding tebal.

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Sumber referensi: Kumar V, Abbas AK, Fousto N, Aster. Pathologic Basis of
Disease. Tenth Edition. Elsevier Saunders. 2017

2.5. Kista Nabothian

Kista Nabothian terbentuk akibat servisitis kronik
oleh karena peradangan yang dapat mengakibatkan
stenosis duktus kelenjar serviks dan terbentuk kista
nabothian yang dilapisi oleh epitel kolumnar.

Gambar 8. Makroskopik kista Nabothian, tampak kista pada permukaan

serviks.
Sumber referensi: Kumar V, Abbas AK, Fousto N, Aster. Pathologic Basis of
Disease. Tenth Edition. Elsevier Saunders. 2017

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2.6. Endometriosis
Menggambarkan adanya kelenjar atau stroma
endometium dalam lokasi abnormal di luar uterus.
Keadaan ini dapat ditemukan pada ovarium, ligamen
uterus, septum rektovagina, peritoneum pelvik,
umbilikus, vagina, vulva dan apendiks.
Secara klinis, gejala endometriosis berupa
dismenore berat dan nyeri pelvik, dan keadaan ini
merupakan penyebab paling sering infertilitas pada
wanita. Fokus endometrium di bawah pengaruh hormon
ovarium dan karenanya mengalami perubahan
menstrual siklik dengan perdarahan periodik.
Diagnosis histologik definitif memerlukan dua dari
tiga gambaran berikut: kelenjar, stroma, endometrium
dan pigmen hemosiderin dalam lesi ektopik.

A B

Gambar 9. Endometrosis. A. Kista endometriosis pada ovarium

mengandung material nekrotik coklat (kista coklat), B. Kelenjar dan
stroma endometrium, banyak terlihat makrofag yang mengandung
hemosiderin.

Sumber referensi: Kumar V, Abbas AK, Fousto N, Aster. Pathologic Basis of

Disease. Tenth Edition. Elsevier Saunders. 2017

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2.7. Leiomioma Uteri
Merupakan tumor tersering pada wanita, terdiridari
massa jinak sel-sel otot polos. Tersering pada wanita
usia reproduktif aktif dan berkaitan dengan stimulasi
estrogen. Secara morfologi, tumor berbatas tegas, bulat,
kenyal, nodul putih kelabu yang timbul dalam
miometrium (intramural), di bawah serosa (subserosa)
atau tepat di bawah endometrium (submukosa). Tumor
tersebut dapat mengalami degenerasi kistik dan
kalsifikasi.
Leiomioma dapat asimtomatik atau dapat berkaitan
dengan perdarahan uterus abnormal, nyeri, kelainan
kandung kemih dan gangguan fertilitas. Transformasi
ganas sangat jarang terjadi.

Gambar 10. A. Uterus dibuka untuk membebaskan tumor di dalam rongga

endometrium dan pada pemotongan terlihat gambaran putih padat.
B. Leiomioma menunjukkan sel-sel yang berdiferensiasi baik, reguler dan
sel-sel otot polos yang berbentuk spindle.
Sumber referensi: Kumar V, Abbas AK, Fousto N, Aster. Pathologic Basis of
Disease. Tenth Edition. Elsevier Saunders. 2017

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2.8. Serous Cystadenoma Ovarii
Merupakan surface epithelial tumor yang bersifat
jinak. Dapat dijumpai pada usia premenarch sampai
postmenopause, tetapi paling sering dijumpai pada
wanita usia reproduktif. Dapat dijumpai bilateral. Pada
pemeriksaan makroskopis, kista dengan ukuran 1-10 cm
(jarang mencapai ukuran 30 cm), yang pada pembelahan
dapat dijumpai kista unilokular atau multilokular,
dinding kista dengan permukaan yang halus tidak
dijumpai adanya penebalan namun terkadang dapat
dijumpai papil, berisi cairan serous. Pada pemeriksaan
mikroskopis, dinding kista dilapisi oleh epitel kolumnar
bersilia menyerupai epitel yang melapisi tuba falopii.
B

Gambar 11 . A. Makroskopis serous cystadenoma tampak kista unilokular,

dinding kista dengan permukaan yang halus. B. Mikroskopis serous
cystadenoma, dinding kista dilapisi oleh epitel kolumnar bersilia
Sumber referensi: Kumar V, Abbas AK, Fousto N, Aster. Pathologic Basis of
Disease. Tenth Edition. Elsevier Saunders. 2017

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2.9. Mucinous Cystadenoma Ovarii
Merupakan surface epithelial tumor yang bersifat
jinak. Dapat dijumpai pada usia premenarch sampai
postmenopause, tetapi paling sering dijumpai pada
wanita usia reproduktif. Biasanya unilateral. Pada
pemeriksaan m akroskopis, ukuran kista bervariasi dari
1 cm sampai dengan ukuran > 30 cm dengan berat bisa
mencapai 25 kg, pada pembelahan tampak kista
multilokular, dinding kista dengan permukaan yang
halus, berisi cairan gelatinous yang lengket. Pada
pemeriksaan mikroskopis, dinding kista dilapisi oleh
epitel kolumnar tinggi, tanpa silia menyerupai epitel
cervix atau intestinal.

A
B
Gambar 12. A. Makroskopis mucinous cystadenoma tampak kista
multilokular, dinding kista dengan permukaan yang halus. B. Mikroskopis
mucinous cystadenoma, dinding kista dilapisi oleh epitel kolumnar dengan
inti yang terletak dibasal.
Sumber referensi: Kumar V, Abbas AK, Fousto N, Aster. Pathologic Basis of
Disease. Tenth Edition. Elsevier Saunders

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2.10. Dysgerminoma
Merupakan germ cell tumor yang bersifat ganas
dengan gambaran morfologi menyerupai seminoma
pada testis. Dapat dijumpai pada dekade kedua dan
ketiga (usia rata-rata 22 tahun). Biasanya unilateral
(80%-90%). Pada pemeriksaan makroskopis,
merupakan tumor yang solid dengan ukuran dari nodul
sampai massa yang besar yang dapat memenuhi rongga
abdomen, pada pembelahan tampak massa homogen
yang berlobus-lobus, berwarna putih sampai kecoklatan.
Pada pemeriksaan mikroskopis, tampak sel-sel
monoton, berukuran besar, polygonal dengan inti bulat,
besar, letak ditengah, khromatin kasar, sitoplasma jernih
sampai eosinofilik, dengan batas antar sel yang jelas.
Sel-sel tersebut tersusun dalam kelompokan-
kelompokan yang dipisahkan oleh jaringan ikat fibrous
dengan infiltrasi sel-sel radang limfosit.

A B
Gambar 13. A. Makroskopis dysgerminoma pada pemotongan dijumpai
massa yang berlobus-lobus, berwarna kecoklatan. B. Mikroskopis
dysgerminoma tampak kelompokan-kelompokansel-sel tumor yang
dipisahkan oleh jaringan ikat dengan infiltrasi sel-sel radang limfosit
Sumber referensi: Kumar V, Abbas AK, Fousto N, Aster. Pathologic Basis of
Disease. Tenth Edition. Elsevier Saunders. 2017
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2.11. Mature Cystic Teratoma (Dermoid Cyst)
Merupakan germ cell tumor yang bersifat jinak
terdiri dari 3 lapisan germ cell. Dapat dijumpai pada
semua usia, 50% pada usia 20-40 tahu. Pada
pemeriksaan makroskopis, tampak kista yang berukuran
< 10 cm dengan permukaan luar yang halus, pada
pemotongan dijumpai kista yang berisi rambut dan
material sebaseus, terkadang dijumpai nodul yang berisi
gigi dan tulang yang menonjol dari dinding kista
(Rokitansky protuberance). Pada pemeriksaan
mikroskopis dijumpai tumor yang terdiri dari berbagai
komponen organ normal. Kulit dan appendages, glia,
peripheral nervous tissue, lemak, tulang rawan, otot
polos dan epitel gastrointestinal merupakan jaringan
yang paling sering dijumpai.

A B
B
Gambar 14. A. Makroskopis dermoid cyst, pada pemotongan dijumpai
rambut dan nodul yang berisi gigi (Rokitansky protuberance). B.
Mikroskopis dermoid cyst, pada dinding kista dijumpai kulit dan komponen
pilocebaseous.

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Sumber referensi: Kumar V, Abbas AK, Fousto N, Aster. Pathologic Basis of
Disease. Tenth Edition. Elsevier Saunders. 2017

3. Prosedur Praktikum
3.1. Alat dan bahan
- Mikroskop
- Slide mikroskopik berupa: Servisitis,
Leiomioma Uteri, Hiperplasia Endometrium,
Serous Cystadenoma Ovarii, Mucinous
Cystadenoma Ovarii, Serous
Cystadenocarcinoma Ovarii.
- Alat tulis
- Atlas Patologi Anatomi
3.2. Cara kerja
- Kuliah overview
- Observasi preparat gross dan micros yang telah
disediakan dengan pembesaran 40x dan 100x.
- Identifikasi slide dengan mengenal jaringan dan
kelainan-kelainan yang dijumpai.
- Deskripsi dan diskusikan kelainan yang tampak
pada sediaan
- Beri keterangan gambar pada lembar tugas
praktikum yang telah disediakan.
3.3. Hasil praktikum
- Tugas praktikum dikerjakan di lembar tugas yang
telah disediakan dan dikumpulkan untuk
dikoreksi oleh dosen yang bertugas

24
 LAPORAN KEGIATAN DIAGNOSTIK
LABORATORIUM PATOLOGI ANATOMI
Jalan Gedung Arca No.53 Medan 20217

NAMA PRAKTIKAN :.....................................................

INSTANSI PRAKTIKAN : ....................................................
ALAMAT PRAKTIKAN : ..................................................
HP/ E-MAIL PRAKTIKAN : .....................................................

HASIL PEMERIKSAAN HISTOPATOLOGI

Gambar hasil pemeriksaan Gambar hasil pemeriksaan

Gambar hasil pemeriksaan Gambar hasil pemeriksaan

25
 Medan, ............................. 2023

PRAKTIKAN LABORAN DOSEN

(..........................) (.............................) (................................)

DAFTAR PUSTAKA
Kumar, V. Cotran, R. S, Robbins, S. L. 2017. Robbins
Basic Pathology. 10th Edition. Philladephia. WB
Saunders Company. New Delhi.

Nucci, M.R,. Olivia, E. 2009. Gynecologic Pathology.

Elsevier Churchill Livingstone.

PathologyOutlines.com.
https://www.pathologyoutlines.com/.

Webpathology. Visual Survey of Surgical Pathology.

https://www.webpathology.com/.

26
 PATOGENESIS NEOPLASMA PADA
PAYUDARA

1. Tujuan Praktikum
Tujuan Umum: Mahasiswa mengetahui gambaran
makroskopis dan mikroskopis dari lesi infeksi dan
neoplasma yang dijumpai pada sistem reproduksi
wanita.
Tujuan Khusus:
1. Mahasiswa mengetahui gambaran makroskopis dan
mikroskopis lesi dari payudara.
2. Mahasiswa mengetahui gambaran makroskopis dan
mikroskopis lesi dari plasenta.
2. Landasan Teori
2.1. Fibroadenoma Mammae
Makroskopik:
- Berkapsul atau berbatas jelas dan mudah digerakkan
- Konsistensi padat kenyal seperti karet.
- Warna abu-abu putih.
- Pada umumnya berdiameter 2 - 4 cm, kadang-
kadang lebih besar.

27
 Gambar 15. Makroskopik Fibroadenoma Mammae
Sumber referensi: http://www.pathologyoutlines.com

Mikroskopik:
- Stroma biasanya halus, seluler, dan sering miksoid,
fibrolastik dengan bagian myxomatik, mirip stroma
intralobuler, mengelilingi kelenjar- kelenjar dan
rongga- rongga kistik yang dilapisi epitel. Komponen
epitelium bisa tertekan dan mengalami distorsi oleh
proliferasi stroma.
- Pada wanita yang lebih tua, stroma lebih padat akibat
hialinisasi dan epitel mengalami atrofi.
- Ada 2 bentuk :
a. Pericanalicular fibroadenoma
Kelenjar berbentuk bulat atau oval.
b. Intracanalicular fibroadenoma
Kelenjar terdesak stroma sehingga tampak
sebagai celah-celah.
28
 Gambar 2. Mikroskopik Fibroadenoma Mammae.
Sumber referensi: Kumar V, Abbas AK, Fousto N, Aster. Pathologic Basis Of
Disease. Tenth Edition. Elsevier Saunders. 2017

2.2. Karsinoma Mammae

Makroskopik :
- Berupa massa tumor, dengan ukuran sampai diameter
10 cm.
- Konsistensi lunak seperti daging.
- Kulit permukaan sering ulseratif.
- Pada irisan:
• Berwarna putih kotor.
• Terdapat daerah-daerah nekrosis dan perdarahan
yang berwarna coklat kehitaman dengan
konsistensi rapuh.

29
 Gambar 3. Makroskopik Karsinoma Mammae.
Sumber referensi: http://www.pathologyoutlines.com

Mikroskopik :
- Terdiri atas sel-sel ganas epithel ductal yang
pleomorfik membentuk kelompok- kelompok
irregular lajur-lajur atau struktur tubular.
- Sel ganas infiltrasi dalam stroma.
- Terdapat sebukan sel-sel lymphosit dalam stroma.
- Banyak didapatkan mitosis yang atypik.

30
 Gambar 4. Mikroskopik Karsinoma Mammae.
Sumber referensi: http://www.pathologyoutlines.com

31
3. Prosedur Praktikum
3.1. Alat dan bahan
- Mikroskop
- Slide mikroskopik berupa: Fibroadenoma
mammae, karsinoma mammae
- Alat tulis
- Atlas Patologi Anatomi
3.2. Cara kerja
- Kuliah overview
- Observasi preparat gross dan micros yang telah
disediakan dengan pembesaran 40x dan 100x.
- Identifikasi slide dengan mengenal jaringan dan
kelainan-kelainan yang dijumpai.
- Deskripsi dan diskusikan kelainan yang tampak
pada sediaan
- Beri keterangan gambar pada lembar tugas
praktikum yang telah disediakan.
3.3. Hasil praktikum
- Tugas praktikum dikerjakan di lembar tugas yang
telah disediakan dan dikumpulkan untuk
dikoreksi oleh dosen yang bertugas.

32
 LAPORAN KEGIATAN DIAGNOSTIK
LABORATORIUM PATOLOGI ANATOMI
Jalan Gedung Arca No.53 Medan 20217

NAMA PRAKTIKAN :.....................................................

INSTANSI PRAKTIKAN : ....................................................
ALAMAT PRAKTIKAN : ..................................................
HP/ E-MAIL PRAKTIKAN : .....................................................

HASIL PEMERIKSAAN HISTOPATOLOGI

Gambar hasil pemeriksaan Gambar hasil pemeriksaan

Gambar hasil pemeriksaan Gambar hasil pemeriksaan

33
 Medan, ........................... 20213

PRAKTIKAN LABORAN DOSEN

(..........................) (.............................) (................................)

DAFTAR PUSTAKA
Kumar, V. Cotran, R. S, Robbins, S. L. 2017. Robbins
Basic Pathology. 10th Edition. Philladephia. WB
Saunders Company. New Delhi.

Macfarlane, P.S., Reid, R., Callander, R. 2000.

Pathology Illustrated, 5th Ed., Churchill Livingstone,
London.

PathologyOutlines.com.
https://www.pathologyoutlines.com/.

Webpathology. Visual Survey of Surgical Pathology.

https://www.webpathology.com/.

34
BAHAN AJAR PRAKTIKUM
PATOLOGI ANATOMI
BLOK GINEKOLOGI
FEMALE GENITAL SYSTEM
ANATOMY OF FEMALE GENITAL SYSTEM
 CERVICITIS

• Etiologi : Gonokokus,Trichomonas vaginalis, Candida

atau Micoplasma
• Servisitis akut yang paling sering ditemukan pasca
partus dan ditandai oleh infiltrasi akut neutrofil di
bawahgaris mukosa.
• Peradangan kronik dapat mengakibatkan stenosis
duktus kelenjar serviks dan terbentuk kista nabothian
yang dilapisi oleh epitel kolumnar.
• Hal ini harus dapat dibedakan dengan dysplasia pada
cervik
 SQUAMOUS CELL CARCINOMA OF THE
CERVIC

• Most common type of cervical carcinoma

• Nearly all cases are associated with high risk human papillomavirus (HPV) and
arise from a precursor lesion, high grade squamous intraepithelial lesion (HSIL)
• Predominantly associated with HPV 16 and HPV 18 (HPV 16 > HPV 18)
• More common in low resource countries and women without adequate
cytologic screening
• Most cases arise at the squamous-columnar junction of the cervix
 SQUAMOUS CELL CARCINOMA OF THE
CERVIC

• High prevalence of HPV infection among adolescents and young women

• HPV 16 is the major causal agent for squamous cell carcinoma, in contrast to
HPV 18 typically associated with endocervical adenocarcinoma
• Most tumors are due to progression of a precursor lesion, HSIL
• Usually spreads through cervical lymphatics to regional lymph nodes or via
direct extension to vagina, uterus, parametrium, lower urinary tract,
uterosacral ligaments; distant metastases may involve aortic and mediastinal
lymph nodes, lungs, bones and adnexa
 GROSS FINDING

• Red, friable, indurated or ulcerated lesion

or elevated granular area in early stage
tumors
• Exophytic, papillary, polypoid, nodular or
ulcerated mass
• Deeply invasive mass with infiltration into
surrounding structures
• Variable size
 MICROSCOPY FINDING

• Tumor cells infiltrating as irregular anastomosing nests or single cells within

desmoplastic or inflammatory stroma
• Stromal loosening, desmoplasia or increased epithelial cell cytoplasmic
eosinophilia in tumors with superficial stromal invasion
• Lymphovascular invasion may be present
• Grading is based on nuclear pleomorphism, size of nucleoli, mitotic activity and
necrosis and does not correlate with prognosis
• Morphologic variants : Keratinizing SCC, Nonkeratinizing SCC, Papillary SCC,
Basaloid SCC, Verrucous SCC, etc
 HIPERPLASIA ENDOMETRIUM

• Proliferation of endometrial glands with a resulting increase in gland to stroma

ratio
• Current system of classification :
• Hyperplasia without atypia
• Atypical hyperplasia / endometrioid intraepithelial neoplasia (AH / EIN)
• Prior terminologies (simple and complex) are no longer included
• AH / EIN is considered a premalignant condition
 • Premenopausal
• Polycystic ovarian syndrome (PCOS): increased circulating androgens peripherally

E •
converted into estrogen
Chronic anovulation / infertility: dysregulated estrogen without opposing progesterone
T secretion → simultaneous proliferation and breakdown
• Peri and postmenopausal
I • Exogenous estrogen:

O • Estrogen supplementation: systemic therapy to alleviate symptoms of menopause

→ endometrial proliferation
L • Tamoxifen: hormonal treatment for breast cancer acts as estrogen receptor
antagonist in breast but agonist in endometrium
O • Any age

G • Obesity: aromatase (enzyme converting circulating androgens to estrogen) is found in

adipose tissue → peripheral hyperestrogenism

Y • Ovarian pathology:
• Stromal hyperplasia and hyperthecosis: stromal luteinization → hyperandrogenism
→ hyperestrogenism
• Hormone secreting stromal tumors: granulosa cell tumor, thecoma
HISTOPATHOLOGY
 ENDOMETRIAL CARCINOMA

• Endometrial carcinoma is the most frequent cancer occurring in the female

genital tract
• Mean age is sixth decade, with a range from the third to ninth decades
• Endometrioid histotype constitutes approximately 80% of all endometrial
carcinomas, most of which are low grade (FIGO grade 1 - 2)
• In rare cases, CA-125 and CEA may be elevated
• IHK : PAX8, CK7, ER / PR and vimentin
 GROSS FINDING

• Mass arising from endometrial surface

with varied appearances / sizes but
usually exophytic and friable in texture
• Tumor / myometrial interface usually
vaguely demarcated, which is useful to
grossly assess depth of invasion during
intraoperative evaluation
• Occasionally, no grossly appreciable mass,
in which case the entire endometrium
must be submitted for histologic
evaluation (if prior biopsy showed
carcinoma / atypical hyperplasia)
 MICROSCOPY FINDING

• Architecture
• Key feature is confluent or back to back glands lacking intervening stroma
• Cribriform or microacinar configurations
• Complex papillary, micropapillary or villoglandular structures
• Cytologic features
• Resembles proliferative type endometrium with varying features / degrees of atypia but cytology must differ
from that of surrounding nonneoplastic glands
• Cellular / nuclear enlargement
• Nuclear rounding (rather than elongation) with large nucleoli
• Loss of polarity
• Cytoplasmic eosinophilia
 SEROUS CYSTADENOMA OF OVARY

• Benign partially or completely cystic lesion measuring > 1 cm in size and

composed of cells resembling fallopian tube epithelium or cuboidal nonciliated
epithelium resembling ovarian surface epithelium
• Usually 3 - 10 cm (but can be up to 30 cm), oval to round, smooth glistening
surface
• Usually watery clear to pale yellow cyst fluid but can be viscous and mucoid
HISTOPATHOLOGY
 MUCINOUS CYSTADENOMA OF THE
OVARY

• Benign mucinous neoplasm composed of cysts and glands lined by

gastrointestinal or Müllerian type mucinous epithelium lacking
architectural complexity or cytologic atypia
• May be associated with mature teratoma or Brenner tumor
• Filled with dense, viscous, sticky, gelatinous material
• Mean size 10 cm, rarely > 30 cm
HISTOPATHOLOGY
 SEROUS CYSTADENOCARCINOMA OF
THE OVARY

• Accounts for majority of ovarian carcinoma diagnoses and related

deaths
• Often bilateral with variable in size; often large, ~30% of cases with
grossly normal ovary or surface nodules < 1 cm
• Exophytic mass with solid or papillary growth and solid areas tan to
white with necrosis and hemorrhage
GROSS FINDING
 MICROSCOPY FINDING

• Solid masses of columnar to cuboidal cells with eosinophilic cytoplasm and slit-
like spaces (fusion of papillae)
• Solid, pseudoendometrioid, transitional cell carcinoma-like (SET) appearance
(more common in BRCA1 mutations)
• Hierarchical papillary branching, glandular and cribriform patterns common
• Significant nuclear atypia and pleomorphism (> 3x variation in size) with large,
bizarre and multinucleated forms, prominent nucleolus, often large and
eosinophilic
• High mitotic index: ≥ 12 mitotic figures per 10 high power fields, often atypical
• Necrosis is frequent
BREAST
 ANATOMY & HISTOLOGY OF BREAST

• Parenchyma : Essential parts of

an organ that are concerned with
its function
• Stroma
- Framework/Supporting tissue of
an organ
- Contains connective tissue&
blood vessel
- Opposite of parenchyma
 FIBROADENOMA MAMMAE

• Kelainan jinak pada payudara yang terbanyak ditemui pada wanita

muda dengan usia < 30 tahun
• Gambaran klinis : tumor padat, soliter, pertumbuhan lambat, terkadang
tanpa nyeri, mobile, nodul berbatas tegas dengan diameter hingga 3 cm,
bisa multiple nodule
• Makroskopis : Massa tumor berbentuk ovoid, berbatas tegas.
Lobulated dengan pemotongan tampak permukaan putih keabuan
• Mikroskopis :
▪ Dijumpai campuran gambaran proliferasi epitel kelenjar dan stroma
▪ Pada komponen epitel, dikenal gambaran Intracanalicular dan
Pericanalicular
GROWTH PATTERN OF FIBROADENOMA
MAMMAE
 INVASIVE BREAST CARCINOMA

• Terminologi Invasive Breast Carcinoma of No Special Type

dikenal juga dengan Ductal Carcinoma
• Merupakan salah satu kanker terbanyak pada wanita
• Berdasarkan WHO, IBC memiliki banyak varian
histopatologi
• Makroskopis:
- ukuran dari 10 mm - >100 mm
- Bentuk irregular, tidak berbatas
tegas
- Pada pemotongan biasanya
tampak “yellow-white streaks”
diantara massa tumor yang
berwarna putih keabuan
• Mikroskopis IBC :
- Terdiri dari sarang-sarang tumor berbentuk cord, sheets, trabeculae dan clusters
- Dijumpai bentuk tubular
- Sel-sel pleomorfik, dengan mitosis atipik yang banyak dijumpai
- Dapat dijumpai kalsifikasi atau pun nekrosis
GRADING HISTOPATOLOGI BREAST
CARCINOMA

• Klasifikasi oleh Bloom & Richardson

dimodifikasi Elston & Ellis
• Grading merupakan suatu prognostic
factor
• Grade 1 = well differentiated
• Grade 2 = moderately differentiated
• Grade 3 = poorly differentiated
 MOLECULAR TESTING BREAST
CARCINOMA

• Ada 3 pemeriksaan molecular

(imunohistokimia) yang menjadi
tes rutin bagi penderita breast
cancer yaitu pemeriksaan
Estrogen Receptor, Progesteron
Receptor dan HER 2
• Pemeriksaan ini dilakukan untuk
tujuan sebagai targeting therapy
 BREAST SELF EXAMINATION

❑The American Cancer Society recommends

that women perform a breast self-examination
once a month.
❑The best time to do a breast self-exam is one
week after your period so that your breasts
will be less tender and you will be more likely
to notice any changes in their look or feel.
❑After menopause, do breast self-exams on the
first day of each month.
THANK YOU
PATHOLOGY OF FEMALE
GENITAL DISORDERS I
dr. Ren Astrid Allail Siregar, M.Ked(PA), Sp.PA
DISEASES OF THE VAGINA
▪ INFECTIOUS INFLAMMATORY DISORDERS
▪ MALIGNANT NEOPLASM
VAGINITIS

• Vaginitis is one of the most common reasons for a patient to visit

her gynecologist, accounting for more than ten million office visits
each year.
• Abnormal colonization or invasive infection has been reported for
practically all major types of organisms, including viruses,
bacteria, fungi, and parasites.
• It is difficult to determine the most common organism responsible
for vaginitis because frequency lists vary according to age, sexual
activity, and method of microbial identification
BACTERIAL VAGINOSIS

• Organisms such as Trichomonas and Candida have long been known

to produce vaginitis; however, until recently there have been a
substantial number of women who have a copious vaginal
discharge or pruritis in the absence of a readily identifiable
pathogen.
• In the past, this condition was designated nonspecific vaginitis,
but the term bacterial vaginosis currently is preferred because
evidence of inflammation is typically absent.
• Gardnerella, a gram-negative bacillus, has been isolated from
women with vaginosis at a higher rate than asymptomatic women
and thus was considered to be responsible for nonspecific vaginitis
• The diagnosis of bacterial vaginosis is made
if three of the following four criteria are
present: (1) homogeneous, thin, malodorous
discharge, (2) vaginal pH 4.5, (3) vaginal
epithelial cells with numerous attached
bacteria (‘‘clue’’ cells), and (4) fishy odor
on alkalinization of vaginal secretions.
• The diagnosis usually is confirmed by
elimination of other pathogens, combined
with identification of gram-negative to
gram-variable bacilli and ‘‘clue’’ cells on
wet mount or smears, or by culture.
MALIGNANT NEOPLASMS

• In contrast to the high prevalence of intraepithelial lesions of the

cervix and vulva, vaginal intraepithelial neoplasia (VAIN) is
relatively rare.
• The reason for this discrepancy is unknown, but may be related to
a lesser susceptibility of the vaginal mucosa to HPV infection than
the cervical transformation zone.
• However, similar to the cervix, the range of HPV types that can
affect this area is greater than those that occur in the vulva.
SQUAMOUS CELL CARCINOMA OF THE VAGINA

• Squamous cell carcinoma (SCC) represents about 80% of malignant

neoplasms primary to the vagina.
• Only 1% of malignant neoplasms of the female genital tract are
classified as squamous cell carcinoma originating in the vagina.
• Clinical features : - painless vaginal bleeding or discharge
- dysuria
• To be considered a primary tumor of the vagina, the neoplasm
must be located in the vagina, without clinical or histologic
evidence of involvement of the cervix or vulva.
• Gross findings :
• Vary in size, > 10 cm
• Lesi polypoid, fungating and
ulceration
Microscopic findings

• SCC of the vagina resemble those arising in the cervix

• Histologically graded as well differentiated (G1), moderately differentiated
(G2), poorly differentiated or undifferentiated (G3)
• Well differentiated tumors have polygonal squamous cells with ample
eosinophilic cytoplasm, abundant keratin pearls and intercellular bridges
• Poorly differentiated tumors have small cells with scant cytoplasm and
hyperchromatic nuclei
• Nuclear pleomorphism and mitotic activity increases from well to poorly
differentiated
• HPV+ tumors are more frequently of nonkeratinizing, basaloid or warty type
than HPV- tumors and more often showed diffuse p16 immunoreactivity
SARCOMA BOTRYOIDES

• The most common malignant neoplasm of the vagina in infants

and children is embryonal rhabdomyosarcoma, most of which is of
the subtype designated sarcoma botyroides
• Most children present with symptoms of a vaginal mass or
bleeding.
• The tumors usually are located along the anterior wall of the
vagina, and appear as papillae, small nodules, or pedunculated or
sessile soft, polypoid masses with an intact overlying mucosa.
Larger tumors may protrude through the introitus vagina.
HISTOPATHOLOGY FINDING

• MACROSCOPY : Soft gray or tan, edematous, and nodular tumors

• MICROSCOPY :
• The presence of a cambium tumor cell layer underlying an intact
epithelium
• The cambium layer is defined as the condensed subepithelial layer
of rhabdomyoblasts that are scattered in a loose myxoid or dense
collagenous stroma
• The tumor cells are of round to spindle shape, with oval nuclei, an
open chromatin pattern, and inconspicuous nucleoli
DISEASES OF THE CERVIX
• CERVICITIS
• BENIGN NEOPLASIA
• PRECANCEROUS LESION
• INVASIVE CANCER
CERVICITIS

• Inflammatory conditions of the cervix are extremely common and

may be associated with a purulent vaginal discharge.
• Infectious cervicitis is the initial event of the pelvic inflammatory
disease.
• Bacterial and chlamydial infections of the cervix are the most
common cause of infectious cervicitis, also HPV and HSV.
BENIGN NEOPLASIA (CERVICAL POLYP)

• Endocervical polyps constitute the most common new growths of

the uterine cervix.
• Cervical polyps are focal, hyperplastic protrusions of endocervical
folds, including the epithelium and substantia propria.
• Cervical polyps are most often found during the fourth to sixth
decades and in multigravidas.
• They may present with profuse leukorrhea due to hypersecretion
of mucus from inflamed endocervical epithelium or abnormal
bleeding from ulceration of the surface epithelium.
Histopathology Findings
• Gross : Most polyps are single and measure from a few millimeters
to 2–3 cm
• Microscopy : cervical polyps display a variety of patterns that vary
according to the preponderance of one or another of the tissue
components.
• It is composed of mucinous epithelium that lines crypts, with or
without cystic changes with blood vessels can predominate
• Squamous metaplasia involving the surface or glandular epithelium
of polyps is frequently observed.
• The supporting connective tissue of polyps is generally loose, with
centrally placed feeding vessels and is almost always infiltrated by
a chronic inflammatory infiltrate.
Endocervical polyp; note the rich vasculature within the central fibrovascular core,
including large, thick walled arteries.
PRECANCER LESIONS OF THE CERVIX

• Most tumors of the cervix are of epithelial origin and are caused
by oncogenic strains of HPV.
• During development, the columnar mucus-secreting epithelium of
the endocervix is joined to the squamous epithelial covering of the
exocervix at the cervical os.
• With the onset of puberty, the squamocolumnar junction
undergoes eversion, causing the columnar epithelium to become
visible on the exocervix.
• The exposed columnar cells, however, eventually undergo
squamous metaplasia, forming a region called the transformation
zone, where tumors most commonly arise.
Pathogenesis

• Sexually transmitted virus, human papillomavirus (HPV), is the

major aetiological factor.
• Most HPV infections are transient and are eliminated within
months by the host immune response
• HPV is detectable by molecular methods in nearly all cases of
cervical intraepithelial neoplasia (CIN) and cervical carcinoma
• Like most other DNA viruses, HPV uses host cell DNA polymerases
to replicate its genome and produce virions
• The E6 and E7 proteins of “high risk” HPV variants inhibit p53 and
RB
• HPV variants are classified as high-risk or low-risk types based on
their propensity to induce carcinogenesis.
• High-risk HPV infection is the most important risk factor for the
development of SIL that can progress to carcinoma. Two high-risk
HPV viruses, types 16 and 18, account for approximately 70% of
cases of SIL and cervical carcinoma
• Low-risk HPV variants (e.g., types 6 and 11) associated with the
development of condylomas of the lower genital tract
SQUAMOUS INTRAEPITHELIAL LESIONS
• SIL may expand horizontally and involve the entire transformation zone
• The size and endocervical distribution of SIL tend to vary directly with
increasing severity of lesion grade.
• SIL is characterized by abnormal cellular proliferation, abnormal
maturation, and cytologic atypia. The cytologic abnormalities include
hyperchromatic nuclei, abnormal chromatin distribution, nuclear
pleomorphism, and increased nuclear : cytoplasmic ratio. Nuclear atypia is
the hallmark of SIL.
• The spectrum of epithelial alterations that comprises SIL was therefore
semiquantitatively classified into three categories: CIN grade 1 – neoplastic,
basaloid cells occupying the lower third of the epithelium; CIN grade 2 –
basaloid cells occupying the lower third to Precancerous Lesions of the two-
thirds of the epithelium; and CIN grade 3 – basaloid cells occupying two-
thirds to full thickness of the epithelium
LOW GRADE SQUAMOUS INTRAEPITHELIAL
LESION (LSIL)

• LSIL is typically seen among women in their early 20s and with no
significant clinical manifestations.
• The diagnosis is established by microscopic examination of biopsy
specimens taken after cytologic interpretation of LSIL or atypical
squamous cells of undetermined significance (ASC-US)
• In LSIL there is usually minimal nuclear atypia in the epithelial
cells residing in the lower third of the epithelium
• Squamous cells with productive HPV infections also frequently
show perinuclear cytoplasmic cavitation or halos that are
accompanied by thickening of the cytoplasmic membrane
cont. LSIL

• The combination of significant nuclear atypia and cytoplasmic

halos has been termed koilocytosis or koilocytotic atypia and is
pathognomonic of a productive HPV infected
• Taken together, the histological and cytological features of
koilocytosis, nuclear atypia, architectural abnormalities, and
multinucleation are pathognomonic of an HPV-infected epithelium
at any site in the lower genital tract and are especially prominent
in LSIL.
HIGH GRADE SQUAMOUS INTRAEPITHELIAL
LESIONS

• In HSIL (CIN 2, 3), atypia should be present in all layers of the

squamous epithelium, but to an extent and degree that exceeds
what is seen in LSIL
• Microscopically, HSIL is characterized by an expansion of the basal
cell population, which shows nuclear enlargement and
overlapping, irregularity in nuclear size, and abnormal mitotic
figures
• Cell borders between the primitive cells are usually indistinct
INVASIVE SCC OF THE CERVIX

• The most common cervical carcinomas are squamous cell

carcinomas (75%), followed by adenocarcinomas and mixed
adenosquamous carcinomas (20%) and small cell neuroendocrine
carcinomas (<5%)
• Molecular, clinical, and epidemiological studies have implicated
HPV infection in the pathogenesis of cervical carcinoma. More
than 90% of cervical carcinoma contains DNA sequences of specific
HPV types, especially HPV 16 and HPV 18.
• The presenting symptoms of patients with invasive carcinoma of
the cervix of all histologic types appear to be dependent on the
size and stage of the lesion
• The most significant and common feature was bleeding following
intercourse or douching
Pathology Finding

• The gross appearance of invasive squamous cell carcinoma varies

widely. Early lesions may be focally indurated, ulcerated, or
present as a slightly elevated, granular area that bleeds readily
• Microscopically, invasive squamous cell carcinoma is characterized
by anastomosing tongues or cords of neoplastic epithelium
infiltrating the stroma
• Individual cells are generally polygonal or oval with eosinophilic
cytoplasm and prominent cellular membranes. Intracellular
bridges may or may not be visible.
Histological Typing
• One of the earliest approaches to classifying cervical squamous cell
carcinomas was based on the predominant cell type. The classification
separated squamous cell carcinomas into large cell keratinizing, large
cell nonkeratinizing, and small cell nonkeratinizing
• Keratinizing carcinomas are characterized by the presence of well-
differentiated squamous cells that are arranged in nests or cords that
vary greatly in size and configuration.
• The defining feature of keratinizing carcinomas is the presence of
keratin pearls within the epithelium, and the presence of a single
keratin pearl is sufficient to classify a tumor as a keratinizing carcinoma.
• Keratin pearls are composed of clusters of squamous cells that have
undergone keratinization and are arranged in a concentric nest.
• The neoplastic squamous cells not forming keratin pearls frequently
have abundant eosinophilic cytoplasm and prominent intracellular
bridges.The nuclei are often enlarged, but mitotic figures are not
numerous
• Nonkeratinizing squamous cell carcinoma is characterized by
nests of neoplastic squamous cells that frequently undergo
individual cell keratinization but, by definition, do not form
keratin pearls.
• The cells have relatively indistinct cell borders. The nuclei tend to
be round to oval with coarsely clumped chromatin. Mitotic figures
are numerous.
• In some cases SCC is composed of solid sheets of cells with clear
cytoplasm
• Some investigators have reported that this classification has
prognostic significance in patients treated with radiotherapy
Microscopic Grading

• The most commonly used grading system for squamous cell

carcinoma is a modification of the original system proposed by
Broders in 1920.
• This method was based on the proportion of the tumor undergoing
keratinization with the formation of squamous pearls and a
number of mitoses.
• Currently histologic grading divides squamous cell carcinomas into
three groups, well differentiated (grade 1), moderately
differentiated (grade 2), and poorly differentiated (grade 3).
• In well-differentiated (grade 1) tumors, the most
striking feature is abundant keratin, which is
deposited as keratin pearls in the center of
neoplastic epithelial nests
• In moderately differentiated (grade 2) squamous
cell carcinomas, the neoplastic cells are more
pleomorphic than in grade 1 tumors, have large
irregular nuclei, and have less abundant
cytoplasm
• Poorly differentiated (grade 3) squamous cell
carcinomas are generally composed of cells with
hyperchromatic oval nuclei and scant indistinct
cytoplasm, resembling the malignant cells of
high-grade SIL
DISEASES OF THE UTERUS
• ENDOMETRITIS
• ENDOMETRIOSIS
• POLYP ENDOMETRIAL
• ENDOMETRIAL HYPERPLASIA/CARCINOMA
ENDOMETRITIS

• Inflammation of the endometrium is classified as acute or chronic

depending on whether a neutrophilic or a lymphoplasmacytic
infiltrate predominates, respectively
• Endometritis is a component of pelvic inflammatory disease and is
frequently a result of N. gonorrhoeae or C. trachomatis infection.
• Histologic examination shows a neutrophilic infiltrate in the
superficial endometrium coexisting with a stromal
lymphoplasmacytic infiltrate.
• Prominent lymphoid follicles may be seen, particularly in
chlamydial infection.
• Tuberculosis causes granulomatous endometritis, frequently with
associated tuberculous salpingitis and peritonitis.
ADENOMYOSIS/ENDOMETRIOSIS

• Adenomyosis refers to the presence of endometrial tissue in the

myometrium.
• Nests of endometrial stroma, glands, or both are found deep in
the myometrium interposed between the muscle bundles.
• This endometrial tissue induces reactive hypertrophy of the
myometrium, resulting in an enlarged, globular uterus, often with
a thickened uterine wall
• Endometriosis is defined by the presence of endometrial glands
and stroma in a location outside the uterus
Pathology Finding
• Endometriosis typically consists of functioning endometrium, which
undergoes cyclic bleeding.
• Because blood collects in these aberrant foci, they appear grossly as red-
brown nodules or implants
• They range in size from microscopic to 1 to 2 cm in diameter and lie on
or just under the affected serosal surface.
• When the ovaries are involved, the lesions may form large, blood-filled
cysts that turn brown (chocolate cysts) as the blood ages.
• With seepage and organization of the blood, widespread fibrosis occurs,
leading to adhesions among pelvic structures, sealing of the tubal
fimbriated ends, and distortion of the fallopian tubes and ovaries.
• The diagnosis depends on finding both endometrial glands and stroma at
sites external to the endometrium.
ENDOMETRIAL POLYP

• Endometrial polyps are common and have been identified in

between 2 and 23% of patients undergoing endometrial biopsy
because of abnormal uterine bleeding.
• Polyps occur in pre- and postmenopausal women and are thought
to be related in some way to hyperestrogenism, possibly
originating as a localized hyperplasia of the endometrial basalis
secondary to hormonal influence
• Polyps may be single or multiple, sessile or broad based,
pedunculated or attached to the endometrium by a slender stalk
• The glands within a polyp are usually endometrioid in type but not
uncommonly exhibit metaplastic change, including ciliated,
eosinophilic, mucinous, and squamous metaplasia
ENDOMETRIUM HYPERPLASIA

• Endometrial hyperplasia (EH) is a pathological condition

characterised by hyperplastic changes in endometrial glandular
and stromal structures lining the uterine cavity
• Most cases of EH result from high levels of oestrogens, combined
with insufficient levels of progesterone
• Unopposed oestrogenic stimulation of the endometrium causes
proliferative glandular epithelial changes, including glandular
remodelling, resulting in variably shaped, irregularly distributed
glands.
• Risk factors for the development of EC include obesity,
unbalanced oestrogen therapy, tamoxifen treatment, PCOs, and
nulliparity
• Endometrial hyperplasia is one of the most frequent causes of abnormal
uterine bleeding, which leads to EC if left untreated.
• In 10% of premenopausal women with abnormal uterine bleeding,
histological findings show endometrial hyperplasia, and in 6% of
postmenopausal women with uterine bleeding EC is found.
• The World Health Organization (WHO) classification, first presently the
most widely used, is a four-tier classification system that takes into
account both cytologic and architectural abnormalities.
• Considering some issues, WHO simplified the classification of
endometrial hyperplasia in 2014 and proposed two categories based
upon the presence of cytologic atypia: Hyperplasia w/o Atypia and
Atypical hyperplasia/ endometrioid intraepithelial neoplasia
ENDOMETROID CARCINOMA

• In the United States and many other Western countries,

endometrial carcinoma is the most frequent cancer occurring in
the female genital tract.
• It generally appears between the ages of 55 and 65 years and is
uncommon before age 40.
• Atypical endometrial hyperplasia/endometrioid intraepithelial
neoplasia (AEH/EIN) is a precursor of endometrioid carcinoma
• In the 4th edition of the WHO classification, endometrial
carcinoma is classified into endometrioid, mucinous, serous, clear
cell, and other types of carcinomas.
• An EIN diagnosis requires that the histological findings meet the
following criteria : 1. The area of the glands exceeds the area of
stroma. 2. When a localizing lesion is present, epithelial cells
within the architecturally crowded focus should be cytologically
different compared to background glands. 3. The area meeting
architectural and cytological criteria must have a minimum size of
1 mm. 4. Exclusion of both benign and malignant mimics
• EIN should be distinguished from endometrioid carcinoma by
recognition of stromal invasion
• In the 4th edition of WHO classification, stromal invasion is
defined as the loss of intervening stroma (a confluent glandular or
cribriform pattern)
Uterus with endometrial tumour, received incised sagitally on the anterior aspect
LEIOMYOMA

• Benign tumors that arise from the smooth muscle cells in the
myometrium are properly termed leiomyomas, but because of
their firmness often are referred to clinically as fibroids.
• Leiomyomas are the most common benign tumor in females,
affecting 30% to 50% of women of reproductive age, and are
considerably more frequent in black women.
• Leiomyomas are typically sharply circumscribed, firm graywhite
masses with a characteristic whorled cut surface.
• They may occur singly, but more often occur as multiple tumors
that are scattered within the uterus, ranging from small nodules
to large tumors
• Some are embedded within the myometrium (intramural),
whereas others may lie immediately beneath the endometrium
(submucosal) or the serosa (subserosal)
• On histologic examination, the tumors are characterized by
bundles of smooth muscle cells mimicking the appearance of
normal myometrium.
• Foci of fibrosis, calcification, and degenerative softening may be
present
LEIOMYOSARCOMA

• Leiomyosarcomas of the uterus virtually always arise de novo from

the mesenchymal cells of the myometrium.
• They are almost always solitary and most often occur in
postmenopausal women, in contradistinction to leiomyomas,
which frequently are multiple and usually arise premenopausally
• Leiomyosarcomas typically take the form of soft, hemorrhagic,
necrotic masses.
• The histologic appearance varies widely, from tumors that closely
resemble leiomyoma to wildly anaplastic neoplasms.
• The diagnostic features of leiomyosarcoma include tumor
necrosis, cytologic atypia, and mitotic activity
 Gross findings of the dedifferentiated leiomyosarcoma
a) Resected uterus was cut longitudinally in the anterior wall and the tumor was exposed. The polypoid tumor was lobulated and
attached to the uterine fundus; b) Sagittal slice of the tumor (above) and horizontal slice of right side (below). On the sagittal
slice, the fascicular area (FA) is to the left and the pleomorphic area (PA) to the right. Dashed line denotes assumed borderline
between these areas; borderline in central necrotic area was postulated from morphology of tumor cells with coagulation
necrosis. A leiomyoma was seen in the posterior uterine wall (arrowhead).
THANK YOU
Pathology of the BREAST
 Anatomy & Physiology
 The areolar tissue: melanin, smooth muscle, elastic fibers.
 Montgomery's areolar sebaceous glands (prevent
chapping) undergo hyperplasia during pregnancy; they are
the little bumps.
 The breast contains about 20 lobes.
 Each lobe is drained by a lactiferous duct.
 Elastic fibers surround the lactiferous ducts and their
branches.
 The lactiferous duct widens to become the lactiferous sinus
underneath the nipple.
One collecting duct
and its terminal
ductules, plus the
accompanying
acinus and stroma, is
called a "lobule".
Lobules → lobes.

The breast contains

about 20 lobes
arranged like the
sections of a half-
orange cut along its
equator.
Normal Breast tissue
 The stroma between the lobes is fibrofatty.
 As a woman gets older, there is usually more fat
relative to stroma in the breast.
 During pregnancy, true secretory units sprout from
each terminal duct, coming to dominate the breast
histology.
 After delivery, milk production (lactation) begins.
Lactation

Before lactation During lactation

 Hormones to remember...

 Estrogen: Develops the large ducts

 Progesterone: Develops the lobules and ductules
("acini")
 Stimulation of the nipple causes production of
both:
◼ Prolactin (which develops the secretory units and
causes milk production)
◼ Oxytocin (which causes the contraction of
myoepithelial cells→ the milk go through the ducts
and come down).
 During the second half of the monthly cycle,
progesterone causes some proliferation of
ducts and stroma in the lobules.
 When the cycle ends, these changes
regress.
 After menopause, the lobules may vanish,
leaving only the larger ducts.
 DEVELOPMENTAL PROBLEMS
 Inverted nipples: common, especially in larger breasts,
and may make nursing more difficult.
◼ If a previously-normal nipple inverts, there is a problem, i.e.,
something has retracted underneath, and it's the stroma of a
cancer until proven otherwise.
 Accesory axillary breast: The extension of normal breast
tissue over the entire anterolateral chest wall into the
axillary fossa.
 Virginal hypertrophy (macromastia): very large breast(s)
developing around puberty.
 Hypomastia: almost complete failure of breast
development.
◼ Around half of these women have mitral-valve prolapse.
 INFLAMMATIONS
 Acute mastitis and breast abscess
◼ Usually occurs during early lactation,
◼ Usually Staph. aureus (abscess), less often streptococcus (spreading
cellulitis).
 Traumatic Fat necrosis
◼ A solid mass, often in a fatty breast tissue, caused by an injury.
◼ Necrotic fat cells surrounded by mixed inflammatory infiltrate, later with
calcification, foreign body reaction, scarring.
 Periductal mastitis (recurrent subareolar abscess)
◼ A hyperkeratinizing squamous metaplasia with inflammation
◼ Almost all these women are smokers.
Fat necrosis
 Duct ectasia
◼ An uncommon cause of a breast mass, usually in older women, usually
tender and with nipple retraction.
◼ Chronic inflammation and fibrosis around ducts are typical.
◼ The ducts are loaded with a lipid-and-macrophage rich material.
◼ The underlying cause is unknown; many of these women turn out to
have pituitary prolactinomas.
 Granulomatous lobular mastitis
◼ All these women have been pregnant.
◼ There is some autoimmune reaction against the secretory units.
◼ Differential diagnosis: Tbc, sarcoidosis, and reaction to a ruptured
implant.
 Galactocele
◼ One or more ducts becomes plugged during lactation.
 Mondor's disease
◼ Thrombophlebitis of the breast.
 FIBROCYSTIC CHANGE
OF THE BREAST

 This is the most common “condition" of breast

 Always multifocal
 The cause is obscure;
◼ Estrogen is a known factor,
◼ Women on the estrogen-progesterone balanced
pills get less fibrocystic change.
Three patterns occur separately or together:
 1. fibrosis
 2. cyst formation (>3 mm)
 3. adenosis.
FIBROCYSTIC CHANGE
OF THE BREAST
 1. Fibrosis
◼ Dense collagenization distorting and
compressing the epithelial structures.
◼ This is most common in upper outer
quadrants, patients in 30's.
 FIBROCYSTIC CHANGE
OF THE BREAST

 2. Cyst formation (>3 mm) :

◼ Dilated dusts containing cloudy serous fluid (sometimes bloody
or infected)
◼ All breasts, during childbearing, contain microscopic cysts.
 They are abnormal when they got larger than 2 mm or so.

◼ Grossly, the blue-dome cyst is very familiar.

◼ Epithelium may be flattened, cuboidal, columnar, or even show
apocrine metaplasia.
◼ Surrounding stroma likely to be fibrous.
◼ Cysts likely to be tender before menses.
FIBROCYSTIC CHANGE
OF THE BREAST
 3. Adenosis:
◼ This extremely common change means
extra, crowded ductules in some of the
lobules.
◼ Often the lumens are a bit distended
("blunt duct adenosis"), but they are not
deformed, compressed or distorted.
Adenosis

Cyst formation

Fibrosis
 PROLIFERATIVE BREAST
DISEASES
 Three entities have been removed from the
"fibrocystic change" category because they confer a
significant cancer risk:
 1. Epithelial hyperplasia
◼ Totally benign-looking hyperplasias
◼ Atypical ductal hyperplasias
◼ Atypical lobular hyperplasia
 2. Sclerosing adenosis
 3. Small duct papillomas
 PROLIFERATIVE BREAST
DISEASES
 Epithelial hyperplasia
 More than the usual two layers of cells in ducts and/or
lobules.
◼ At least one layer will be myoepithelial cells.
 Epithelial hyperplasia is usually an incidental finding, and
does not produce a mass.
 Cells are piled up and may even fill ducts and/or ductules.
 Most often, there is a mixed population of cells.
◼ Epithelial cells,
◼ Myoepithelial cells.
 ALERTS
 Atypical hyperplasia:
◼ If there is some anaplasia of architecture (swiss
cheese) or cells (with ugly nuclei).
◼ The cells do not fill the ducts or acini ("in-situ
cancer“).
 Carcinoma in situ (CIS):
◼ CIS is only slightly more likely to progress to invasive
cancer than is "atypical hyperplasia."
 Atypical epithelial hyperplasia:
◼ Great risk of breast cancer.
Epithelial hyperplasia
 PROLIFERATIVE BREAST
DISEASES

 Sclerosing adenosis
 Proliferation of small ductules and sometimes even acini in
a fibrous stroma
 Usually it's a tender lump in the upper outer quadrant.
 Patients are usually around age 30-40.
 This mimics cancer both clinically and microscopically:
◼ (1) There'll always be myoepithelium, expressing smooth-muscle
actin, S100, high MW keratin antigens.
◼ (2) The normal lobular architecture is preserved, though lobules
may be expanded (under low-magnification).
◼ (3) Sclerosing adenosis can be solitary, but it never cuts "gritty"
like many breast cancers.
Sclerosing adenosis
 PROLIFERATIVE BREAST
DISEASES
Radial scar
 It is a star-shaped fibrosing lesion that looks like a
typical crablike cancer on mammography
 Benign on biopsy
 No increased risk for cancer!
Small duct papillomas
 Seldom produce masses.
 These possess fibrovascular cores, with epithelial
hyperplasia-type lesions.
 FIBROADENOMA
 The most common benign breast tumor,
 Occurs at any time during reproductive life,
◼ most often under age 30.
 It presents a small, sharply circumscribed,
freely movable nodule within the breast
substance.
 A loose stroma surrounds ducts that are often
crushed flat.
Fibroadenoma
 Phylloides tumor
 Cystosarcoma phylloides
 "Phylloides" means "leaves", referring to the
artichoke-like appearance of many of these
tumors
 Exhibits metaplastic and/or anaplastic stroma
and supposedly rapid growth
 If it metastasizes, it will be as a sarcoma
Phylloides tumor
 LARGE DUCT PAPILLOMA

 Intraductal papilloma
 This is a small (less than 1 cm) lesion in a
major duct just below the nipple.
 It produces bloody nipple discharge.
 Occasionally it causes nipple retraction.
 Radiology (galactogram): injecting dye into
each of the lactiferous sinuses.
Intraductal papilloma
 CARCINOMA OF THE
BREAST
 This is the most common cancer in women
 It is rare before age 25,
◼ more common with increasing age.
 Around 1 in 9 women will develop breast cancer during
their life.
 Breast cancer usually presents as a dominant, painless
mass.
 Nowadays it is often found on mammography long before
symptoms appear.
 Risk factors
 Female gender
◼ 100x as common as in men
 Ethnic group
◼ Ashkenazi (a Jewish ethnic group) ancestry (the effect is explained by
the high prevalence of BRCA1 mutations in the Ashkenazi population)
◼ Every ethnic group has a high incidence of breast cancer; American
Indians have the least.
 Geography
◼ The US and Northern Europe have the highest rates
 Increasing age
◼ breast cancer is rare before age 25
 Obesity
◼ supposedly; "synthesis of estrogens in fat deposits"
 Longer reproductive life: Estrogen
◼ menarche before age 13 or menopause after 50
 Nulliparous women or those having their first child at a
late age (over 30)
 Family history of breast cancer
◼ father's side as well as mother's
 History of high-dose radiation
◼ atom bomb survivors, women radiated for breast abscesses
◼ Hodgkin's disease treatment only in younger women
 History of epithelial hyperplasia (especially Atypical)
 Previous breast cancer
 Previous cancer of the endometrium
 Alcoholism
◼ because of folic acid deficiency

 Previous fibroadenoma
◼ triples the risk

 Genetic Factors: Germ line mutations in BRCA1 and BRCA2,

p53 (Hereditary breast-ovarian cancer syndrome) ATM
gene(Ataxia Talengiectasia), 10q locus in Cowden Syndrome.
 Estrogen replacement
◼ as a risk factor for breast cancer after menopause remains
controversial.
 NONINVASIVE (“in situ")
CARCINOMA
 Non-invasive, but they may form masses by filling ducts
and/or lobules.
 Ductal carcinoma in situ (DCIS)
 Comedocarcinoma
 Solid DCIS
 Cribriform DCIS
 Papillary DCIS
 Micropapillary DCIS
 "Paget's disease of the nipple"
 DCIS with microinvasion
 Non-infiltrating (in situ) lobular "carcinoma" .
 Ductal carcinoma in situ ("DCIS")
This is the most commonly-identified
lesion on mammography.
These lesions are usually unilateral,
they often present around for decades,
and probably only a minority ever
invade.
 Comedocarcinoma
 The most common
 Solid intraductal proliferation, central necrosis
 Unlike the other "DCIS" lesions, the cells of
comedocarcinoma are usually quite anaplastic and vary
widely in size.
 Often the necrotic cores calcify, making them easy to spot
on mammography.

Solid DCIS
 Simply fills ducts.
 The cells are monomorphic and monotonous.
Comedocarcinoma
 Cribriform DCIS
 Swiss-cheese appearance.
Papillary DCIS
 Looks like the papillary lesions of proliferative breast disease, with
fibrovascular cores, but has a monomorphic cell population.
Micropapillary DCIS
 It is little mounds of cells along the wall without fibrovascular cores.
Paget's disease of the nipple
 Intraepithelial growth of large, pale, mostly-single cancer cells in the
nipple.
 Breast looks inflamed (misdiagnose: "eczema of the nipple“)
 There is most often an underlying duct carcinoma.
 DCIS with microinvasion
 Usually is comedocarcinoma with invasive cancer confined to 1 mm
away from the ducts.
Non-infiltrating (in situ) lobular "carcinoma"
 This is a distinctive proliferation of tame-looking cells, slightly larger
than normal, filling the ductules of one or more lobules.
 The lobules are expanded but not distorted.
 Often there are signet-ring cells.
 It heralds infiltrating ductal or lobular carcinoma; however, the invasive
cancer is just as likely to be in the opposite breast.
 "Lobular CIS" is usually an incidental finding when tissue from the
breast is excised and examined for some other reason.
 If you get a chance to examine both breasts, it's usually bilateral.
 INFILTRATING (invasive)
BREAST CARCINOMA
 Invasive ductal carcinoma
◼ No Special Type (NST)
◼ Medullary carcinoma
◼ Mucinous (colloid, gelatinous) carcinoma
◼ Adenoid cystic
◼ Papillary carcinoma
◼ Tubular carcinoma
◼ Metaplastic cancers

 Infiltrating lobular carcinoma

 Invasive ductal carcinoma
No Special Type (NST)
 Usual type;
 About 75% of infiltrating ductal carcinomas.
 Most of these are
◼ stellate or micronodular,
◼ quite hard (scirrhous),
◼ on cut section:
 a chalky-white look flecked with yellow (elastin bands),
 produces the gritty sensation of cutting an unripe pear.

 Microscopy (scirrhous carcinoma):

◼ cells often arranged in nests or cords or streams
◼ a very desmoplastic stroma.
Invazive ductal carcinoma (Scirrhous)
Invasive ductal carcinoma
Invasive ductal carcinoma
Medullary carcinoma
 Big, bulky, and soft.
 Lymphocytes are plentiful among the
tumor cells.
 The prognosis is slightly better than that
of other types.
 This type of cancer is much-
overrepresented among women with
mutated BRCA1 syndrome.
 Mucinous (colloid, gelatinous) carcinoma
◼ Clumps of cells in lakes of mucin.
◼ Grossly, the tumor is a gelatinous mass.
Adenoid cystic carcinoma
◼ Very low aggressiveness in the breast.
Papillary carcinoma
◼ Arises from the large ducts.
Tubular carcinoma
◼ Best prognosis for any breast carcinoma
◼ Grossly: star-shaped
◼ Microscopy: microglandular structures plus impressive desmoplasia
Metaplastic cancers
◼ Usually with cartilage
◼ The cell of origin is myoepithelium.
Colloidal (mucinous) carcinoma
Papillary Carcinoma
Tubular Carcinoma
 Infiltrating lobular
carcinoma
 10% of infiltrating breast cancer.
 The cells tend to be very small and to lack
much anaplasia:
◼ often include signet-ring cells
◼ making circles around the ducts.
 Such tumors are often multifocal within a
breast, and are often bilateral.
 Lobular carcinoma is infamous for spreading to
the arachnoid and to bone.
 Localization of Breast Cancers

 A majority of breast cancers arise in the outer

quadrants, particularly the upper outer quadrant,
 Left breast is slightly more often affected than the right
one.
 The single most important prognostic indicator in a
case of breast cancer is the size of the tumor at
presentation.
 The presence or absence of metastatic tumor in the
axillary lymph nodes is even more important.
 Prognosis & Metastases
 Cancers detected by self examination (very good
prognostic indicator, but very few women perform self-
examination properly)
 Tiny cancers found only on mammography, with no
palpable mass.
 Clinical course: The disease is likely to metastasize, but is
often indolent, and late recurrences are common.
 Metastases:
◼ Regional lymph nodes
◼ Brain
◼ Bone
◼ Other organs (lung, liver, opposite breast, skin).
Spread of Breast Carcinoma
Tis- Carcinoma-in-situ
T1 - Gross size of tumor is less than 2.0 cm
diameter
T2 - Gross size of tumor is between 2-5 cm
diameter
T3 - Gross size of tumor is above 5 cm diameter
T4 - Tumor of any size involving chest wall or skin

N0 - No axillary node involved

N1 - Metastases to axillary nodes that are freely
mobile
N2 - Metastases to fixed (immobile) axillary nodes
N3 - Metastases to internal mammary nodes

M0 - No metastases outside of local nodes

M1 - Metastases present
 Diagnosis
 nipple retraction
 calcification (around 60%
calcify to some extent; many
benign lesions also calcify)
 retraction and dimpling of
skin
 edema of overlying skin or
arm
 lymphedema of breast
(lymphangiitis
carcinomatosa; peau
d'orange, orange-peel)
 fixation to chest wall or
overlying skin
 ulceration of overlying skin
 satellite nodules in
overlying skin
 "inflammatory
carcinoma" (heavy
invasion of breast skin
veins, causing congestion).
Calcification
Inflammatory carcinoma (peau d’orange)
Lymphovascular invasion
DISEASES OF THE
MALE BREAST
 Gynecomastia
 Men’s breast doesn’t contain lobules!!!
 Proliferation of a man's ducts and stroma, unilateral or bilateral.
 Causes:
◼ Idiopathic (adolescents or older men; due to XXY)
◼ Hyperestrinism (liver cirrhosis, tumors, iatrogenic, female
impersonators, guys using anabolic steroids to look more
masculine).
◼ Other drugs
 digitalis
 spironolactone;
 soy products (contain natural estrogens).
 Idiopathic gynecomastia has no risk for cancer
◼ XXY's and female impersonators (trans-sexuality) on estrogens are at
increased risk.
 The severity is widely variable.
Gynecomastia in male breast
 Carcinoma of the male
breast
 Uncommon
◼ 100x less common than in women,
◼ XXY's and female impersonators (trans-sexuality) on
estrogens are at increased risk (20X).
 It is almost always an infiltrating ductal carcinoma,
usually without much desmoplasia.
 Remember: men’s breast doesn’t contain
lobules!!!
THANK YOU