University of Arizona



Pathology Study Guide:Intraepithelial Neoplasm Staging:I: Limited to upper epitheliumLimited to upper 2/3 of epitheliumInvolving full thickness of the epitheliumUterine Pathology:Dysfunctional Uterine Bleeding: Abnormal bleeding (Amenorrhea, dysmenorrhea, menorrhagia, metrorrhagia, oligomenorrhea) due to functional causes. PCOSHypothalamic/Pituitary/Gonadal DisordersOvarian LesionsHypothyroidismAbnormal Uterine Bleeding: Abnormal bleeding due to organic causesDiseaseClinical PresentationGross PathologyMicroscopic PathEtiologyOther InfoBenign Neoplasms/Non-Neoplastic EntitiesLeiomyoma- MOST COMMON TUMOR IN WOMENAbnormal bleeding, mass, asymptomatic, dystociaWell circumscribed gray whorled nodule(s)Mature smooth muscle with rare mitoses. Well circumscribedHeightened sensitivity to estrogenNot a pre-malignant lesionEndometrial hyperplasiaAbnormal uterine bleeding4 types: Simple wo/atypiaSimple w/atypiaComplex wo/atypiaComplex w/atypia(Complex=gland packing with abnormal shape)Prolonged estrogen exposureOften found in conjunction with ovarian tumors, PCOS, HRT, etc. Lesions with atypia have a 2-30% chance of becoming carcinoma.EndometriosisCyclic dysmenorrhea, menorrhagia, infertility, dyspareuniaChocolate cysts on the surface of ovaries, uterine tubes, peritoneal structures, Presence of normal endometrial tissue outside of the uterusUnknown: Some combination of genetic, hormonal, and immune factors.Theories: Regurgitation, metaplasia, lymp/vascular spread, mechanical implantation.AdenomyosisColicky dysmenorrhea, menorrhagia, dyspareunia, pelvic painChocolate cysts embedded in the uterine myometriumPresence of irregular nests of endometrial stroma (with or without glands) in the myometriumUnknownEctopic PregnancyAcute abdomen, pelvic pain, shock-like state, missed period hCGPlacental tissue, amniotic sac, and fetal tissue outside the uterusPlacental tissue, amniotic sac, and fetal tissue outside the uterusExtrauterine implantationPredisposing Factors: PID, chronic salpingitis, adhesionsMolar PregnancyComplete MoleUterine size larger than expected, vaginal bleeding, passage of “grape like” structures, hCGMass of thin-walled friable semi-translucent cystic “grape-like” structures involving entire chorionHydropic villous swelling with diffuse trophoblastic proliferationFertilization of an empty ovum by two sperm or a single sperm whose genetic material replicates (karyotype 46XX or 46XY fully paternal)10% become invasive, 2% become choriocarcinoma, Tx, curettage or hysterectomyPartial MoleUterine size larger than expected, vaginal bleeding, passage of “grape like” structures, hCGMass of thin-walled friable semi-translucent cystic “grape-like” structures not involving entire chorionPartial villous hydropic swelling with focal syncytiotrophoblastic proliferation, amniotic and fetal parts may be presentFertilization of an ovum by a diploid sperm, or two sperm (Karyotype 69XXX, or 69 XXY)Rarely become aggressive or recurrent Tx, curettage or hysterectomyInvasive MoleRecurrent vaginal bleeding, irregular uterine enlargement, hCGHemorrhagic mass adherent to the uterine wall or invading the uterine wall.Persistence of molar pregnancy after evacuation, benign in nature, locally invasive, Tx chemotherapyMalignant NeoplasmsChoriocarcinomahCG, late postpartum bleeding, bloody and sometimes smelly vaginal discharge, moderate uterine enlargementVERY hemorrhagic mass invading the uterine wallProliferation of cytotrophoblasts and syncytiotrophoblasts with absence of villous formation, marked cytologic atypiaMalignant transformation of chorionic structureExquisitely sensitive to chemotherapy, risk factors: >35 yo, increasing parity, OCP, very aggressive and widely metastasizingPlacental site trophoblastic tumorPostpartum or post-abortion abnormality, hPLDiscrete mass within the myometriumProliferation of intermediate trophoblast at implantation site (polygonal cells)10% disseminate and result in deathCarcinoma (type I) 85% of endometrial carcinomasAbnormal bleeding with or without enlarged uterusDiffuse or polypoid masses within the uterine wallEndometrioid patterns of cells invading the myometriumProlonged estrogen exposure, obesity, EIN, P10 mutations.Stage I & II surgery w/radiation gives 95% 5 year survival. Drops to 50% for stage III & IV. Often found concurrently with ovarian neoplasms.Carcinoma (type II)Abnormal bleeding with or without enlarged uterusMasses within the uterine wallClear cell, serous, and carcinosarcoma (both squamous and adenoid hyperplasia)P53 mutationsWorse prognosis than type ILeiomyosarcomaAbnormal bleeding or uterine massBulky mass with hemorrhageTumor of abnormal smooth muscle cells that show nuclear pleomorphism UnknownGrading of Uterine Cancers: <5% solid area5-50% solid area>50% solid areaStaging of Uterine Cancers:Remains in body of uterusInvades cervixInvades adjacent structuresInvades extrapelvic structuresFallopian Tube Pathology:Suppurative salpingitis: 60% Caused by N. gonorrhea. Causes PID. Outcome: Tubal ovarian abscess.Tuberculous salpingitis: Caused by M. tuberculosis. Classic micro. path.: caseating granuloma.Paratubal Cyst: Benign lesion, translucent cyst filled with clear fluid.Adenocarcinoma: Hard to distinguish primary tubal tumors from secondary ovarian lesions. Presents as watery or bloody discharge. Has to satisfy certain criteria:Dominant tubal massInvolvement of the tubal lumenArising from tubal mucosaExcluding ovarian or peritoneal cancersBreast Pathology:Non-proliferative Proliferative without atypia proliferative with atypia Carcinoma in-situ CarcinomaDiseaseClinical PresentationGross PathologyMicroscopic PathEtiologyOther InfoFibroadenoma (benign)Well circumscribed mass that is freely movable, rubbery, and hormonally responsiveFreely movable, grayish white, rubbery noduleWell circumscribed fibrous myxoid stroma and fibrous dilation of ducts with bi-layered epithelium (different from FCC)No increased risk for malignancyPhyllodes Tumor (benign)Small to large multilocular mass that is “leaf-like”Bulbous protrusions with slit-like spacesStromal overgrowth, infiltrating margins, and great cellularityCan be high grade and aggressiveFibrocystic change (nonproliferative change)Lumpy bumpy tenderness that increases with the luteal phase of menses and abates with menstruationCyst formation with fibrosis and adenosis (and often apocrine metaplasia with single layered glands)Hormonal imbalance and end-organ insensitivityNo increased risk for malignancyProliferative change without atypiaIncidental finding on biopsy or mammographic abnormalityEpithelial hyperplasia, sclerosing adenosis, complex sclerosing lesions, papillomas, fibroadenoma1.5-2X increased risk for malignancyAtypical ductal hyperplasia (proliferative change with atypia)Small unilateral mass or mammographic abnormalityResembles DCIS (no invasion through basement membrane) but not qualitatively or quantitatively8-10X increased risk for DCISAtypical lobular hyperplasia (proliferative change with atypia)Usually an incidental findingResembles LCIS (no invasion through basement membrane) but not qualitatively or quantitatively4-5X increased risk for LCISDuctal carcinoma in-situSmall unilateral mass or mammographic abnormalityDuctal hyperplasia that does not extend beyond the basement membraneIncreased estrogen exposure, family history80% of CIS in the breast. 30% increased risk for invasive carcinomaLobular carcinoma in situIncidental finding, can be bilateral.Acini filled with non-cohesive small cellsIncreased estrogen exposure, family history30% increased risk for invasive carcinomaPaget’s diseaseHyperemia, edema, oozing and ulceration from the skin of the nippleDCIS extending from the ductal cells into the nipple and areola. “Paget cells” can be seen that DO NOT invade the basement membraneHormonal, environmental, and genetic factors50-60% chance of finding ipsilateral, contralateral, or bilateral carcinomaDuctal carcinoma (NST)Pain, breast mass, nipple discharge, mammographic abnormalityFirm non-mobile gritty mass that is infiltrating and retractedTubules, nests, cords, and sheets of pleomorphic cellsHormonal, environmental, and genetic factors79% of invasive breast cancer, metslymph nodes, lung, pleura, and bone, inflammation worsens prognosisLobular carcinomaMass/density in a small %, mostly vague thickening or mammographic abnormality, can be bilateralHard with irregular marginsSingle-file “marching” poorly cohesive tumor cells frequently infiltrating around ductal structuresHormonal, environmental, and genetic factorsMetslymph nodes, peritoneum, retroperitoneum, meninges, GI, ovaries, and uterus, inflammation worsens prognosisMedullary carcinoma (2%)Fleshy and well circumscribedSolid syncytium-like sheets of pleomorphic cells with lymphocytic infiltrateBetter prognosis than NSTMucinous carcinoma (2%)Circumscribed, slowly growing, gelatinous massClusters and islands of cells floating in lakes of mucin pushing into stromaBetter prognosis than NSTTubular carcinoma (10%)Usually detected as mammographic densities (VERY SMALL TUMORS)Well formed tubules without myoepithelial layerExcellent prognosisPapillary carcinoma (1%)Can be bilateralFirm non-mobile gritty mass that is infiltratingPapillary arrangement of ductal carcinomaBetter prognosis than NSTMajor Prognostic Factors:In-situ VS InfiltratingLocal aggressivenessLymphatic spreadDistant metastasisSize of tumorInflammatory?Minor Prognostic Factors:Histologic subtypeNuclear gradeEstrogen and progesterone receptorsHer2/neu expressionLymphovascular invasionProliferative rateDNA contentStaging:DCIS/LCIS<2cm –nodes<5cm +nodes OR >5cm>5cm +nodesDistant metsProstate PathologyDiseaseClinical PresentationGross PathologyMicroscopic PathEtiologyOther InfoProstatitisDysuria, retention, dribbling, purulent discharge, abscessesEdema, redness, ulcerations, abscesses, purulence.PMN or lymphocytic infiltrate, purulent exudate, or granuloma formationAcute: E. coli, klebsiella, enterobacter, serratia.Chronic: any acute cause or abacterialGranulomatous: TB, cocci, BCG, crypto, blasto, non-specific (keratin).Benign prostatic hypertrophy (90% of men >70)Associated with compression of the urethra: retention, dysuria, dribbling, hesitance, nocturia. PSANodularity of the transitional zone not often felt on digital rectal examNodularity, stromal hyperplasia, and glandular hyperplasia with maintenance of basal and luminal cells (High MW cytokeratin stain to determine)Androgen (DHT)Tx: alpha blockers, 5-alpha reductase blockers, TURPConsequences: bladder hypertrophy, cystitis, hydronephrosis, pyelonephritis, urethritis. Not associated with increased risk of malignancyProstatic intraepithelial neoplasm (PIN)Usually asymptomaticNoneHyperplasia of luminal cells without disruption of glandular structure (doesn’t invade basement membrane)UnknownPrecursor lesion to carcinomaProstatic carcinoma (70% of men >70)Associated with compression of the urethra: retention, dysuria, dribbling, hesitance, nocturia, PSAYellow-white, gritty, and firm mass, often not distinguishable from normal prostateProliferation of small glands that is of luminal origin ONLY with cytologic atypia possibleUnknownNote staging and grading scale below. Tx. T I & II-Radical prostatectomy, TIII+ requires radiation and hormone therapy (LH agonist), metastasisobturator nodes, BONE (osteoblastic lesions)Gleason grading scale:Grade lesions within prostate on a scale of 1-5Add two most common grades (IE 3+4)>7=Bad prognosisStaging prostate cancer:T:Tumor1: incidental finding2: confined to prostate(a. unilateral small, b. unilateral large, c. bilateral)3: Invades capsule (a. unilateral, b. bilateral, c. invades seminal vesicle)4: Invades contiguous organsM: Mets0: No mets1: MetsN: Nodes0: no nodal involvement1: nodal involvementUrethra/Penis/Scrotal Pathology:Congenital/acquired urethral defects:Priapism: Pathologic engorgement of corpus cavernosa with bloodPeyronie’s DZ: Banana penis disease (fibrosis of tunica vaginalis)Phimosis/Paraphimosis: Constriction of foreskin behind/in front of glans penisHypo/Epispadias: Congenital development of the urethra with the opening on bottom/top of penis (rather than in glans)DiseaseClinical PresentationGross PathologyMicroscopic PathEtiologyOther InfoUrethritisPurulent discharge, dysuriaPMN infiltrate with/without presence of organisms demonstratedN. gonorrhea MOST COMMON, chlamydia, trichomonas, E. coliCan lead to Reiter’s syndrome: “Can’t see (conjunctivitis), can’t pee (urethritis), can’t climb a tree (arthritis). Autoimmune origin (HLA-B27).BalanoposthitisNonspecific infection of the glans penis with pain, erythema, and possible ulcerationNon-specific: Staph/strep, tinea, candida, Specific: HSVII, HPV 6, 11. Condyloma Acuminatum (benign)Painless raised verrucous areas on the glans/penisRaised red scaly excrescences Branching papillary architecture with koilocytosis in surface layers indicative of viral infectionHPV 6 and 11No increased risk of malignancyBowen’s Disease, Erythroplasia of Queyrat (precancer)White scaly/red shiny patches on the penis with or without ulcerationWhite scaly/red shiny patches on the penis with or without ulcerationMalignant epithelial cells within the epithelium that do not invade the basement membraneHPV 16 and 18These lesions ARE PRECANCEROUSPenile squamous cell carcinomaPainless, slow growing warty mass with or without ulcerationNests, cords, or sheets of abnormal appearing epithelial cells that invade beyond the basement membraneSignificant association with lack of circumcision, smoking, and high-risk sexual behaviors. Metastasisinguinal iliac lymph nodesTesticle and epididymis pathologyCauses of testicular atrophy: (will see Leydig hyperplasia)Estrogen exposureExogenous testosteroneMalnutritionMedicationsCryptorchidismAtherosclerosisHypopituitarismKlinefelter’s DiseaseClinical PresentationGross PathologyMicroscopic PathEtiologyOther InfoCryptorchidismFailure of testicles to descend from abomenPoorly understoodOutcomes: Infertility, 5-10X increase in germ-cell cancers, atrophy. Tx: Orchiopexy.Torsion (MEIDCAL EMERGENCY)Rapid onset of intense testicular pain Blue/black hemorrhagic testicleHemorrhagic infarct with fibrosis, extravasation of RBC’s, venous infarction.Infants: UnknownAdolescents: Bell-clapper abnormalityOrchitisPainful inflammation of the testicle(s)Often subsequent to infection of another proximal structure. Non-specific: Staph/strepSpecific: N. gonorrhea, syphilisGranulomatous: Non-infectious or M. TBGerm Cell Tumors/SeminomatousSeminoma (female counterpart: dysgerminoma)Testicular mass, hyperechoic on ultrasonography. Stains PLAP (Placental Alkaline Phosphate) +Grey, cream, or pale homogenous lobulated mass with well-defined borderUniform population of seminoma cells arranged in sheets or clusters with lymphocytic infiltrateIsochromosome of the short arm of chromosome 12Exquisitely radiosensitive. Metastasispara-aortic lymph nodes.Spermatocytic seminomaTesticular massSoft well-circumscribed mass with bulging cut surfaceNon-cohesive tumor cells similar in morphology to seminoma, but without lymphocytic infiltrateIsochromosome of the short arm of chromosome 12Exquisitely radiosensitive. Metastasispara-aortic lymph nodesNon-Seminomatous Germ Cell Tumor (NSGCT)Yolk sac tumor (NSGCT)Testicular mass. Stains FP +Non encapsulated pale gray gelatinous tumor with or without necrosisLace-like arrangement of cells, with Schiller-Duval bodies.Isochromosome of the short arm of chromosome 12Good prognosis. Metastasispara-aortic lymph nodesEmbryonal carcinoma (NSGCT)Testicular mass. Stains CD30 +Soft, gray, granular mass with or without necrosis and is not well demarcatedPrimitive gland formation with large irregular cellsIsochromosome of the short arm of chromosome 12Grows relatively fast so may be painful. Metastasispara-aortic lymph nodesChoriocarcinoma (NSGCT)Testicular mass. Stains hCG+Hemorrhagic nodule with rim of fibrous tissueMalignant syncytiotrophoblast and cytotrophoblast cells without villous formationIsochromosome of the short arm of chromosome 12Metastasispara-aortic lymph nodes. Very aggressive tumor that is widely metastasizingTeratoma (NSGCT)Testicular massPresence of cartilage, hair, bone, fat, CT, etc can be seen. Well circumscribed tumorOne cell type from every embryonal lineage found. Can be mature (cartilage, fat, bone, etc), or immature.Isochromosome of the short arm of chromosome 12Metastasispara-aortic lymph nodes. Prognosis is good when found in pre-pubertal boys. Post-puberty, all teratomas have malignant potential.Stromal TumorsLeydig cell tumor (functional stromal tumor)Testicular mass, gynecomastia, and precocious puberty may be seen. Androgen and estrogen concentrations in serum.Well circumscribed, often encapsulated, small massesHyperplasia of normal Leydig cells with some cytologic atypia.Isochromosome of the short arm of chromosome 12Metastasispara-aortic lymph nodes. 10% are malignantSertoli cell tumor (stromal tumor)Testicular massLobulated, well circumscribed mass with focal hemorrhageHyperplasia of normal Sertoli cells often forming tubules with a basement membraneIsochromosome of the short arm of chromosome 12Metastasispara-aortic lymph nodes. 10% are malignantGonadoblastoma (stromal tumor)Testicular mass Mixture of stromal and germ-cell components46X/46XY mosaicismMetastasispara-aortic lymph nodes. Germ cell components can become malignant and become seminomasLymphoma (stromal tumor) MOST COMMON TESTICULAR TUMOR >60 Y/OTesticular mass Stains CD45, CD19 and CD20+Poor distinction from surrounding testicular tissueDiffuse large B-cell lymphomaIsochromosome of the short arm of chromosome 12Metastasispara-aortic lymph nodes. Bad prognosisSeminomatous tumors:3rd-4th decadeMetastasize lateExquisitely radiosensitiveLymphatic spreadNon-seminomatous germ-cell tumors (NSGCT):2nd-3rd decateMetastasize earlyRadioresistantHematogenous + lymphatic spreadOvarian PathologyDistinctions:Cystadenoma: Benign with single layer glandular proliferationLMP: Low malignant potential tumor with stratification of glandular structuresCystadenocarcinoma: Malignant tumor with areas of glandular and solid architecture with cytologic atypiaDiseaseClinical PresentationGross PathologyMicroscopic PathEtiologyOther InfoEpithelial Tumors (65-75% of ovarian cancers. Seen in older women)Serous (cystadenoma, LMP cystadenoma, and cystadenocarcinoma)Adnexal mass with or without tenderness, bloating, ascites, abdominal pain. Stains CA125+.Serious filled cystic dilation of the ovary with areas of solid tumor proliferationSerious filled cystic spaces lined by tall columnar ciliated epithelium of various stratifications + psammoma bodies.Risk Factors: #1-Family history, long reproductive span, nulliparity, increased estrogen exposure. DECREASED RISK WITH OCP USE.Mucinous (cystadenoma, LMP, cystadenocarcinoma)Same-these tumors can be VERY large and bilateral. Stains CA125+.Larger cystic masses than seen in serous, filled with mucinMucin filled cystic spaces lined by tall columnar epithelium of various stratification + psammoma bodies. Can be intestinal or endocervical type.SameEndometrioid adenocarcinomaSame. Can be bilateral.Solid or cysticTubular glands resembling endometrial primary tissue present in the ovarySameAssociated with uterine endometrioid neoplasm, endometriosis, and clear cell carcinoma of the ovaryClear cellSameVacuolated cells forming glands, papillae, or sheets. “Clear cells”.SameAggressive tumor with 50% 5 year survival wo/mets, and 0% 5 year w/mets.Brenner tumorSameFibrous stroma with nests of transitional epitheliumSameGerm Cell Tumors (15-20% of ovarian cancers. Seen in younger women)ChoriocarcinomaSame. Stains + for hCG.Hemorrhagic tumorSyncytio/ Cytotrophoblast hyperplasia without villous formationSameVery aggressive tumor usually of placental origin that often has metastasized when identifiedTeratomaSame. Can be bilateral.Can be cystic (dermoid) or solid containing multiple tissue typesMature or immature combinations of tissue types from each of the three embryonal cell layersParthenogenetic eventDysgerminoma (sister to seminoma)SameSolid, nodular, and rubberyPrimitive cells with nests and sheets of homogenous cells with lymphocytic infiltrateSameAggressive but responsive to chemotherapyEndodermal Sinus Tumor (AKA Yolk Sac Tumor)Same. Stains + for FP.Loose gelatinous stromaSchiller-Duval bodiesSameStromal Tumors (Wide age range)Granulosa/Theca cell tumorSame. Causes precocious puberty in young women and endometrial hyperplasia with possible carcinoma in older womenYellowish hormone-producing tumorsCall-Exner bodies (coffee bean nuclei)SameOften seen in conjunction with endometrial hyperplasia/ carcinomaLeydig/Sertoli cell tumorSame. Causes masculinization due to hyperandrogenism: hirsutism, acne, etc.Yellowish hormone-producing tumorsResemble granulosa/theca tumorSameKrukenburg TumorBilateral tumor, usually with colicky painSignet ring cell gastrointestinal carcinoma within both ovariesBenign LesionsFollicular cystLarger cysts can cause pelvic pain, adnexal mass and tendernessCystic dilation of follicle that is smooth and glistening with clear serous fluid contentAttenuated inner granulosa, luteinized theca.Unruptured graafian follicle, ruptured follicle that sealed immediatelyLuteal CystLarger cysts can cause pelvic pain and adnexal masses with tendernessCystic dilation of CL that has a yellow surface and bloody fluid contentLuteinized theca and granulosa cellsPolycystic OvariesElevated LH, androgens, and estrogen, IDDM, hirsutism, Ovarian enlargement, thickening of the cortex, cortical cystsMultiple follicular cysts with inner granulosa and outer theca layersUnknownIncreases risk of endometrial cancerPseudomyxoma Peritonei: Extension of ovarian mucinous tumor into peritoneum (implants), location of choice-appendix.Vagina/Vulva/Cervical PathologyDZCausePathologyClinical Presentation/OtherInflammatory CervicitisN. gonorrhea, C. trachomatis, herpesvirusInfectionPIDCondyloma acuminate (vulva, vagina, or cervix)HPV 6,11Papillary structure with outer koilocytosis due to presence of viral particles in cellsGenital wartsBartholin cystBlockage of outflow tract of Bartholin glandMass located adjacent to vulvaLichen sclerosus (vulva)Autoimmune origin, not well understood.Atrophy and fibrosis of the dermis of the vulva with thinned epidermisPale gray parchment like transformation of the vulva. Associated with increased risk of vulvar carcinoma.Lichen simplex chronicusItching, rubbing, or scratching the vulvaAcanthosis of the squamous epitheliumLeukoplakia of the vulvaCarcinoma in-situ (VIN, VAIN, and CIN). Pre-cancerous lesions.HPV 16,18Malignant transformation of vulvar, vaginal, or cervical surface epithelium that does not breach the basement membrane. Stage I, II, or III depends upon involved thickness of epithelium.CIN: Aceto-white lesionsVIN/VAIN: Lesions mimic Bowen’s disease of the penis being white and scaly or red and velvety with or without ulceration.Paget’s diseaseUnknownLarge neoplastic cells within the epidermis and appendagesPruritic, red, sharply demarcated lesion of the labia majora. RARELY associated with underlying carcinoma.Squamous cell carcinoma (vaginal, vulvar, or cervical)HPV 16,18Invasion of abnormal sheets, cords, and nests of epithelium with nuclear atypia.Can present as fungating, ulcerating, or infiltrative lesions of the vulva, vagina, or cervix. Other pathologies to note: Malignant melanoma of the vulvaAdenocarcinoma of the vaginaEmbryonal rhabdomyosarcoma of the vagina (infancy and early childhood)Staging of Cervical Cancer:CINConfined to cervixExtends beyond cervixExtension into pelvis/vaginaStaging is different for: Uterine, breast, cervical, and prostate cancers. ................
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