DUB: DefState of abnormal uterine bleeding dt functional Endometrial carcinoma: MC invasive cancer of fem CIN/SIN: DefPecancerous lesion that

rous lesion that may exist in the nin

abnormality rather than organic lesions of uterus. genital tract. Type 1Risk factorsobese fem, invasive stage as long as 20 yrs and shed abnorm cells that can
Causes1.Anovulatory cycle(MC):Persistence of graffian diabetic, HTN, nulliparity. Mutation in PTEN Tum suprr be detected by cytological examintn. Associated with high risk
follicles without ovulation. Persistant estrogen prodn with no gene, mutation in PIK3CA gene, KRAS gene and B HPV. MorphCIN I: Possess indistinguishable histology from
progesterone 2. Inadequate luteal phase:Ovulation occurs but catenin oncogene. Microsatellite pathway.Gross condylmata acuminate. It may be raised associated with low risk
functional corpus luteum is inadequate. 3. Persistant luteal Localizes polypoid tumor invol. Entire endometrial virus or flat condyloma ass with high risk virus. Nuclear change
phase: Prolonged functioning of corpus luteum leads to excess surface Micr Well def gland pattern closely accompanied by cytoplasmic halos(koilocytic atypia) CIN II:
secretory glands. resembling norm endometrial lining thus endometroid Appearance of atypical cells in lower layers of sq epithelium with
carcinoma. 3 grades: grade 1:well differentiated, easily persistant differentiation towards prickle and keratinizing
recognized glandular patterns which shows layers.Atypical cell show:Changes in karyocytoplasmic ratio, loss
Endometriosis: DefPresence of endometrial glands and
stroma in normal location outside uterine cavity. SitesOvaries, stratification and cellular atypia. Grade 2: .sim to well of polarity, abnorm mitoses. CIN III: progressive loss of
uterine ligaments, culde sac, pelvic peritoneum, large and small diff along with mixes solid sheets of malignant differentiation accompanied by greater atypia in more layers of
cells.. ..grade3: solid sheets of cells with barely epithelium. GrossNo specific picture is assoc wth cellular
bowels, appendix, laparotomy scars. Patho1.Regurgitation
recognizable glands and greater degree of atypia found in dysplasia/carc in situ except that changes begins
theory:Retrograde menstruation through fallopian tube 2.
Vascular/lymphatic dissemination 3. Metaplastic theory: Same atypia&mitotic activity.Type 2: Etio rare than type1, at squamous columnar junction/transitional zone.
origin of endometrium and mullerian duct(Coelomic epithelium) thin physique, mutant in P53 gene chiefly and also
PIK3CA grossLarge bulky tumors deeply invasive to Carcinoma of cervix: etioloHPV(DNA virus) high risk HPV 16,
4. Other: genietic, hormonal, immune Morph gross: 1.
Nodules with red blue to yellow brown(Gun powder nodules) myometrium. MicrMC histologic type serous 18 Risk factorsMultiple sex partner, young age at first
beneath the serosal surface in site of involvement 2. Organizing carcinoma and less hist type is clear cell& malign intercourse, high parity, persist inf with a high risk oncogenic
hemorrhages cause extensive fibrous adhesion between tubes, mixed mullerian tumor. The precursor lesions, HPV(16&18) GrossArises fron squamo-columnar junction. 3
ovaries and obliterate poich of douglas. 3. Ovaries distorted by endometrial intraepithelial carc,consist of malign cless dist patterns:1. Fungating(commonest &is cauliflower like
identical to serous carc. But remain confined to gland groeth), 2. Ulcerating 3. Infiltrative MicroscopicSCC are
cystic masses filled with brown fluid forming chocolate
surf. Invasive lesion:Papillary growth pattrn.
cyst/endometriomas Micros: Foci of endometrial glands and composed of nests and tongue of malignant sq epithelium with
stroma, old & new hemorrhages, hemosiderin laden mainly large cells which may be:
macrophages &surrounding zone of inflammation and fibrosis

Adenomyosis: DefPresence of endometrial tissue in uterine Leiomyoma:Def benign neoplastic prolifn of smooth
wall Gross uterus may be slightly/markedly enlarged Cut mscl arising from myometrium. Gross Sharply
sectiondiffuse thickness of uterine wall with presence of circumscribed,discrete, round, firm, gray white tumors
coarsely trabecular and ill defined areas of hemorrhages. found wthin myometrium of body of uterus in few
Micros 1.Reveal irregular nests of endometrial stroma w/o cases in lower uterine segments, cervix or uterine
glands arrangd within myometrium sepr from stratum basalis by ligaments. Amy occur within myometrium(intramural),
at least 2-3mm. associated with muscle hypertrophy. 2. just beneath endometrium(Submucosal) or beneath
Shedding of endometrium during mens. Cycle leds to hemorr serosa(Subserosal). Characteristc whorled pattrn of
with adenomyotic nests. Smth muscl bundles on cut section. MicrComposed
of whorled bundles of sm mscles admixed with
variable amnt of CT resembling inv myometrium.
Endometrial hyperplasis/EIN:defIncreased proliferation of
Individual msl cell are uniform in size&shape with
endometrial glands relative to stroma, resultin in increased
charactc oval nucleus& slender bipolar cytoplasmic
gland to stroma ratio when compared to normal proliferative
process. No mitotic figures. Pathological appearance
endometrium. EtiologyDue to prolonged estrogenic
stimulation of endometrium Morphology 4 types: 1. Simple may be alt by sec changes like hyaline degenration,
cystic degenrn, infarct, necrosis, fatty chang.
hyperplasia w/o atypia: AKA cystic mild hyperplasis.
ComplicnAbn bleeding impaired fertility, in pregnant
Characterized by glands of varying size and irregular cystic
spontaneous abortion& postpartum hemrhg
dilation. Occurs dt persistent estrogenic stimulation and on
withdrawal of estrogenic stimultn. Mitoses not prominent. 2. Ectopic preg: defImplantatn of fetus in any site othr
Simple hyperplasia with atypia:Uncommon. Charracerized by than a normal intrauterine locatn. SitesFallopian
appearance of simple hyperplasia but with cytological atypia tubes(90%), ovary, abdominal cavity predisposing
within glandular epithelial cells as defined by loss of polarity, condnPrior pelvic inflammatory disease, peritubal
vascular nuclei. adhesion.

3. Complex hyperplasia w/o atypia: Char by increase in size and
no. of endometrial glands, marked gland crowding &Branching
pf glands with little intervening stroma. Abundant mitotic
figuees +nt. 4. Complex hyperplasia with atypia: Similar to well
differentiatd endometrial adenocarcinoma. Characterised by
incr in no.& size of endometrial glands with crowding
enlargement and irr shape dt cell stratificatn and nuclear
enlargement.
Infertility: Def A disease of repr system defind by failure to
achieve a clinical pregnancy after 12 mnts/more of regular
unprotected sexual intercourse. Cause1. Ovulatory
disorders:PCOS, hypothalamic pituitary failure, thyroid
dysfunctn, hyperprolactemia 2. Fallopian tube blockage:scarring
dt infection, endometriosis, tubal malformtn 3. Uterine factors:
Fibriods, adenomyosis, cervical polyps 4. Cervical factors:
Abnorm cervical mucus/presence of sperm immobilizing abs in
cervical mucus 5. Vaginal fac: vaginal atresa 6. Overwt/underwt
` carcinoid 3. Dysgeminoma 4. Yolk sac
Pathogenis1. Ovarian preg: presumed to result frm 1. Keratinizing pattern 2. Non keratinizing pattern 3. Poorly
rare fertilization and trapping of ovum within the differentiated. Small proportion with small cell undifferentiated
follicle just. 2. Abdominal pregnancies:May dev when carcinomas. Adenocarcinoma: proliferation of glands into
fert ovum fails to enter/drops out of fimbriated end of cervical stroma. Glands are comp of malignant endocervical cells
tube. with large, hyperchromatic nuclei& mucin depleted cytoplasm.
Ovarian tumor classificnA Suface epithelial Teratoma: defRefer to a grp of complex ovarian tumors having
tumors 1. Serous tumors:Benign cystadenoma, various cellular or organoid components reminiscent of normal
serous borderline tumor, serous adenocarcinoma 2. derivatives from more than 1 germ layer. Divided into 3
Mnucinous tumors:Benign cystadenoma, mucinous categories: Mature, Immature and monodermal. Mature
borderline timor, mucinous adenocarcinoma 3. teratoma morphgross:10-15% of cases bilateral, are unilocular
Endometrioid tumors: benign cystadenoma, cyst containing hair & cheesy sebaceous material C/S: thin wall
endometrioid borderline tumors, endometrioid lined by opague, graywhite, wrinkled epidermis fron which hair
adenocarcinoma. 4. Clear cell tumors:benign, shafts freqntly protrude micros:cyst wall composed of stratified
borderline, clear cell adenocarcinoma 5. sq epithelium with underlying sebaceous glands, hair shafts. Also
Transitional:Brenner, brenner tumor of borderline structures from other germ layers can be identified as cartilage,
malignance, malignant brenners. B.Sex cord stromal bone, thyroid tissue&neural tissue. 1% go malign transfrmn.Eg:
tumors:Granulosa tumors, fibromas, fibrothecomas, thyroid carcinoma, melanoma, SCC. Immature teratomas
sertoli cell tumor, leydig cell tumor, gynandroblastoma morph gross: bulky& have smooth external surface C/s:have
C. Germ cell tumor: 1. Teratoma:immature, solid str with areas of hemorr and necrosis. Hairs, sebaceous
mature(solid, cystic) 2. Monodermal(Struma ovaruu, material, cartilage, bine may be +nt. Micr:Varying amount of
imature neuro epithelium, cart, bone. Grows rapidly&frequently
tumor(endodermal sinus tumor) C. penet capsule.
MalignantMetastatic cancer from non ovarian
primary Colonic, appendiceal, gastric, breast.
 Yolk sac tumor: AKA endodermal sinus tumor Fibroadenoma of breast: Benign tumor of fibrous& epithelial
Dysgerminoma:Ovarian counter part of seminoma of testis GrossNonencapsulated, C/S: homogenous, yellw- elements arising from intralobular stroma.MC tumor of fem
grossUnilateral, most are solid tumors ranging in size barely white mucinous appearance Micros: Variable breast. Gross Frequently bilateral and multiple. Grow as
visible nodules to masses that virtually fill entire abdomed growth pattrn:microcystic, macrocystic, solid, spherical nodules usually circumscribed& movable. Well
C/SShows yellow white to gray pink appearance and is ften papillary, glandular or cord. Cells small cuboidal to
capsulated C/SReveals firm. Gray white nodules that buldge
soft and fleshy. MicrosAll malignant tumors. Cells are flattened. SCHiller-Duval above surrounding tissue MicrThe delicate, cellular myxoid
dispersed in sheets/cords sep by scanty fibrous stroma. Fibrous bodies(50%):resembleendodermal sinuses. Present stroma resembles norm intrerlobulr stroma. Epithelium may be
stroma infiltrated with mature lymphocytes and occasional within and outside cytoplasm are eosinophilic, hyaline
surrounded by stroma/comprr/distorted by it. 2 types of pattern:
granuloma. Synciotrophoblastic giant cells may be evident. Tum like globules in which AFP & Alpha1 antitrypsin can be
1. INtracanalicular pattern:Stroma compresses the ducts so that
cells are uniform large vesicular having clear cytoplasm, well demonstrated by immunocytochemical staininig. they are reduced to slit like cleft by ductal epithelium. 2.
defined boundaries and central nuclei. Pericanalicular pattern:Charac by encircling masses of fibrous
Bowenoid papulosis: Occurs in sexually active adults. stroma around ducts. The fibrous stroma may be cellular/mayb
with areas of hyalinised collagen. The adenoma composed of
Hydatidiform mole:Characterized by abnormal placenta with Also related to HPV16 infectn. Rerely develops to
acini with ecretory activity is lactating adenoma.
features: 1.Enlarged, oedematous and hydropic chanfe of invasive carcinoma. GrossPresence of multiple,
chorionic villi which becomes vesicular 2. Variable amount of pigmented(reddish brown) popular lesion.
trophoblastic proliferation. 2 types Complete mole : Results MicrosEpidermis shows prolifrtn with numerous Phylloides tumor: Arise from intralobular stroma. Majority are
from fertilization of egg that has lost its chromosomes and mitoses, some are atypical. Cells are dysplastic with etected as palpable masses. GrossTumors vary in few cm to
genetic material is completely paternally derived. hyperchromatin nucleus & lacks orderly maturation. massive lesions involving entire breast. Round to oval, bosselated
morphology:GrossUterus is enlarged and filled with delicate, Dermal-epidermal border is sharply delineated by an and less fully encapsulated than fibroadenoma. C/S: grey ewhite
friable mass of thin walled, translucent, cystic, grape like intact basement membrane. with cystic cavities, area of hemorrhage, necrosis and
structures with hydropic villi. degenerative changes. MicrLarger lesions have bulbous
MicrosAbnormality in almost all villous tissue. Chorionic villi
BPH/BNH: Extremely common disorder in men over Protusions(leaflike) dt precence of nodules of proliferating
enlarged, scalloped in shape with central cavitation and lack age of 50 yrs characterized by hyperplasia of prostati, stroma covrd by epithelium. In some tumors protusions extend
adequate developed vssls. Extensive trophoblastic stromal and epithelial cells, resulting in formtn of into cystic space. Low grade resembles fibroadenomas but are
proliferation.Implantation site displays atypia.Partial mole : large, fairly discrete nodules in periurethral region of more cellular &contain mitotic figures. Hif=gh grade may be
Results from fertilization of ann egg with sperms. morph: prostate leading to retention of urine & difficulty in difficult to distinguish from oth soft tissue sarcomas & may have
grossUterus is smaller than that of complete mole and micturition Aetiopathogenesis:Androgens play major foci of mesenchymal differentiation.
contains some cystic villi. Fetal parts commonly present. role. Androgen not oonly increase cellular prolifrn but
MimcrosVillous enlargement and architectural disturbance in also inhibit cell death which leads to accumulation of Paget’s disease of breast: Is ecxematoid lesion of nipple, often
only portion of villi. Trophoblastic proliferation is moderate.senescent cells in prostate leading to hyperplasia. ass. With invasive/ non invasive ductal carcinoma of underlying
Main androgen is DHT, formed by conv of testosterone breast. Gross Skin of nipple and areola is crusted, fissured&
Hydrocele:Abnormal collection of serous fluid in some part of by enzyme typeII 5alpha reductase being located ulcerated. Sero-sanguinous fluid oozes from the erosions.Micr
entirely in stromal cells. DHT acts in autocrine fashion
processus vaginalis, usually tunica vaginalis . It is usually Pagets cell lying single/ in cluster in epidermis. Cells are spherical,
on stroma cells or in oaracrine manner by diffusing
painless. Testicle palpable within the larger than epidermal cells, hyperchromatic eith cytoplasmic
into nearby epithelial cells. DHT binds to andr R on
hydroceleTypes1.Congenital halos. Pagets cells are adenocarcinoma typ cells. Underlying
nucleus and form stable complex, which leads to
hydrocele:Vaginal,infantile,congenital, hydrocele of cord. 2.
activation of transcript of androgen dependent genes. brest contains inv/non inv duct carcinoma.
Acquired hydrocele:Primary idiopathic, secondary.
Growth factors life Fibroblast GF, TGF cause prostatic Tumors of breast classify: A.Epithelial tumors1. Benign:Non
growth GrossProstate is enlarged weighing 60- proliferative breast dis, proliferative &Atypical hyperplasia. 2.
Testicular tumors: 1. Germ cell tumorA. Seminomatous: 100gm, is nodular, smooth and firm. Modular Malignant: ductal carcinoma in situ, lobular carcinoma in situ,
Seminoma, spermatocytic seminoma B.Non seminomatous enlargement may compress urethra to slit like orifice. microinvasive carcinoma, intraductal papillary neoplasm, invasive
tumors:Embryonal carcinoma, yolk sac tumor, choriocarcinoma, C/SNodules with primarily glandular prolifrtn are ductal cell carcinoma, invasive lobular carcinoma. B.
teratoma, polyembryoma 2.Sex cord stromal tumors:Leydig cell yellow pink with soft consistenct and white milky fluid Mesenchymal tumors1Benign:Hemangioma, lipoma,
tumor, granulosa cell tumor, ertoli cell tum, Mixed 3.Combined oozes out. MIcrHallmarkis nodularity, the neurofibroma, schwannoma 2. Malignant: Liposarcoma,
germ cell sex cord stromal tumors:Gonadoblastoma 4.Other: composition ranges from stromal fibromuscular angiosarcoma, osteosarcoma C.Myoepithelial
Malignant lymphoma. nodules to fibro epithelial nodules with glandular tumors:myoepitheliosis, Adenomyoepithelioma. D.
predominance. Small to large cystically dilated glands Fibroepithelial tumors:Fibroadenoma, phyllodes tum E. Tumors
lined by 2 layers:Inner columnar and outer of nipple Nipples adenoma, pagets dis of nipple
Seminoma: MC type of germ cell tumor. GrossProduces bulky cuboidal epithelium. Histologically foci of lymphocytic F.LymphomaNon hodgkin’s lymphoma G. Secondary
masses(10x normal testis) and tends to maintain normal contour aggregates, small area of infarction, corpora amylacea metastatic tumors-->Mammary from contralateral breast
as it rarely invades tunica albuginea. Homogenous, gray white, +nt. carcinoma.
lobulated,cut surface usually devoid of hemorr& necrosis.
MicComposed up of uniform cells divided into poorly Fibrocystic disease of breast: MC benign breast Breast carcinoma Aetiopathogenesis: Risk factors 1. Non
demarcated lobules by delicate septa of fibrous tissue conditn producing lumpy breast rather than palpable modifiable:Age (Occurs in older fem age grp, not before 25), Age
containing mod. amount of lymphocytes. Seminoma cells are lumen in breast. CharacteristicsCystic dilation of of menarche(increased risk when earlier), Age at 1st live
large, round to polyhedral&have distinct cell memb, a terminal ducts, Relative increase in interlobular fibrous birth(decrease risk when earlier as pregnancy leads to terminal
clear/watery appearing cytoplasm and large central nucleus. The tissue, variable degree of epithelial proliferation in differentiation, 1st degree relatives with breast carcinoma,
cytoplasm contains varying amnt of glycogen. Approx 15% terminal ducts. increased risk with evidence of atypical hyperplasia 2.
seminomas contain syncytiotrophoblasts.
Fibrocystic changes:Non proliferative breast changes. Modifiable:Radiation(incr risk), Estrogen exposure(increase
Includes formation of cysts f varying sizes and increase incidence ), Carcinoma of contra-lat breast, env toxins like
Spermatocytic seminoma: Rare slow growing germ cell tumor soin fibrous stroma. Cyst formed by dilation of organochlorudes with estrogenic effects, breast feeding when
it doesnot produce metastases. GrossSoft,pale gray, C/S obstructed collecting ducts. Morphology 3 principal practiced longer decrease risk, Abesity decrease risk.
reveals mucoid cysts. MicrLacks lymphocytes, granulomas or morph changes: 1. Cystic change with apocrine The major risk factors are hormonal and genetics. Hereditary
syncytiotrophoblast .Contains Three cell prp 1. Med sized cells, metaplasia: in gross large cyst translucent bluish breast cancer is mainly dt mutation in autosomal dom tum
most numerous, round nucleus& eosinophilic cytoplasm 2. color(blue dome cyst). Cyst contains thin serous to suppressor gene i.e BRCA1&BRCA2, others also like CHEK2, p53,
Smaller cells with round narrow eim of eosinophilic cytoplasm hemorrhagic fluid. 2.Fibrosis: Cyst frequently rupture, PTEN,ATM. Sporadic breast cancer attributed to horm exposure
3.Scattered giant cells, uninucleate/multinucleate. releasing secretory material to stroma. 3. Adenosis: mainly estrogen.
Defined as increase in no. of acinar lobule. Acini
vvvvkddkDnKDUhnCiD enlarged but not distorted. Calcification ocassionally
+nt.
Invasive ductal carcinoma: MC histologic pattern in breast
cancer. Gross: More freq in left breast, often in upper quadrant.
Retraction of nipple& attachment of the tumor to underlying
chest may be +nt. Tumors are firm, hard and have an irregular
border.When cut/scrapped,, they typically produce a
characteristic grating sound dt small, central pin point foci or
streaks of chalky white. C/S:Grey whitw to yellowish white
chalky streaks extending irregularly surrounding fat.
MicroscopWell diff tumor shows prom tubule form, small
round nuclei and rare mitoses. Mod. Different tumors have
greater degree of nuclear pleomorphism& contains mitoses.
Poorly diff carcinomas often invade as ragged nests, or solid
sheets of cells with enlarged irregular nuclei.