path womens - formatted Flashcards

Question

25. 19.02.76 Chorionic villus sampling at 11/40 reveals trisomy 7 (seven). Mother decides to continue pregnancy and routine USS at 18/40 shows viable fetus with normal morphology. Most likely explanation is ? Rob p701 1. Trophoblast margin sampled 2. Mosaicism confined to the placenta 3. Trisomy 7 has bowel and palatal defects not visible on US 4. Trisomy 7 associated with hydrops and fetal death in third trimester

Answer 1

2. Mosaicism confined to the placenta • Confined placental mosaicism o more recently discovered cause of IUGR o documented in up to 2% of viable pregnancies studied by chorionic villus sampling at 9 to 11 weeks' gestation. o Chromosomal mosaicism, in general, results from viable genetic mutations occurring after zygote formation. o Depending on the developmental timing and cell of origin of the mutation, variable forms of chromosomal mosaicism result. o For example, genetic mutations occurring at the time of the first or second postzygotic division result in generalized constitutional mosaicism of the fetus and placenta. o Conversely, if the mutation occurs later and within dividing trophoblast or extraembryonic progenitor cells of the inner cell mass (approximately 90% of the time), a genetic abnormality limited to the placenta results--confined placental mosaicism o The phenotypic consequences of such placental mosaicism depend on both the specific cytogenetic abnormality and the percentage of cells involved. o Chromosomal trisomies, in particular trisomy 7, are the most frequent abnormality documented.

Answer 2

3. Tubular carcinoma commonly incites a prominent desmoplastic response. (Desmoplastic stroma prominent) 26. 42.APRIL02 Which of the following statements concerning invasive breast carcinoma is most correct? 1. "Indian-filing" of neoplastic cells is a classical histological feature of medullary carcinoma.(invasive lobular carcinoma) 2. Bilateral tumours are most likely to occur with colloid carcinomas. (invasive lobular carcinoma) 3. Tubular carcinoma commonly incites a prominent desmoplastic response. (Desmoplastic stroma prominent) 4. Invasive lobular carcinoma accounts for about 30% of invasive breast carcinoma. (5-10%) 5. Monoclonal proliferation of epithelial and myoepithelial cells is a feature of invasive ductal carcinoma. (no myoepitheal component; benign epithelial proliferations require both cell types to be present)

Answer 3

4. As a group, colloid carcinomas have a poorer prognosis than ductal carcinoma of no special type: FALSE - (60% 30 year survival for colloid, < 20% for infiltrating ductal (“no special type”)) 27. 34.APRIL02 Which of the following statement is LEAST correct concerning breast cancer prognosis? 1. Invasion through the lymph node capsule indicates a poorer prognosis than simple node involvement alone (Macrometastases vs micrometastases (< 0.2 cm) and invasion through capsule also NB) 2. If there is no lymph node involvement 10 year survival rates are 70 to 80% (20 – 30% patients with negative nodes may suffer recurrences and die within 10 years 3. If the breast cancer is smaller than 1 cm there is a greater than 95% year survival. (if <2cm 96% 5 YS) 4. As a group, colloid carcinomas have a poorer prognosis than ductal carcinoma of no special type (60% 30 year survival for colloid, < 20% for infiltrating ductal (“no special type”)) 5. Tumours of poor grade have a significantly worse prognosis than tumours of high grade (87% grade I vs 13% grade III)

Answer 4

• Diffuse Growth In Characteristic ‘Indian File’

Answer 5

• All of them can be!! ? bad recall *LW: i think micro papillary is a form of invasive ductal ca, while papillary is only under DCIS subtype? I am likely wrong however.... *AJL - Papillary breast cancer is definitely a thing. All of them are a thing, though the most controversial may be bladder (not explicited listed in the table in robbins but then is alluded to in the text)

Answer 6

2. Stage II Stage 0 - DCIS or LCIS Stage I - Invasive Ca < 2cm (including CIS with microinvasion), no LN or distant mets Stage II - 5cm, involved but≤ mobile axillary nodes, no distant mets; or > 5cm without LN or distant mets Stage III - >5cm with nodes; or any size with fixed axillary nodes; or ipsilateral internal mammary nodes; or with skin involvement, pectoral & chest wall fixation; or clinical inflammatory Ca, if no nodes Stage IV - Any form with distant mets (including ipsilateral supraclavicular nodes)

Answer 7

2. Ductal – NOS (< 20% 30YS) • 74% 30YS for DCIS, • 60% 30YS for lobular, papillary, medullary, colloid (“special types”) • < 20% 30YS for infiltrating ductal (“no special type”) even worse for metaplastic and micropapillary • Lifetime risk for ovarian cancer approximates 30% in BRCA1 carriers – serous cystadenocarcinomas

Answer 8

3. Distinguished from cancer as does not cause compression and distortion of acni (Acini compressed and distorted centrally, and characteristically dilated peripherally) • This lesion is characterized histologically by increased numbers of distorted and compressed acini. • Small lesions commonly present as mammographic calcifications, and larger lesions may form mammographic densities or, rarely, palpable masses. • The acini are compressed and distorted in the central portions of the lesion but characteristically dilated at the periphery. • On occasion, stromal fibrosis may totally compress the lumens to create the appearance of solid cords or double strands of cells lying within dense stroma, a histologic pattern that at times verges on the appearance of carcinoma • Although long thought to be a completely innocuous lesion, sclerosing adenosis has been shown to confer a slightly increased risk of subsequent cancer

Answer 9

3. Increase risk of ductal and lobular SCS: Radiopaedia. Lobular carcinoma in situ is a high-risk marker for the future development of invasive carcinoma. A woman with LCIS has approximately a 15-30% chance of developing an infiltrating ductal or lobular carcinoma in the breast in which the LCIS is discovered or in the contralateral breast. Approximately 20% (range 18-25%) of cases diagnosed with LCIS at core needle biopsy were upgraded to more invasive cancer pathologies at surgical excision. Therefore when LCIS is discovered on a needle biopsy specimen, an excisional biopsy should be performed • Women diagnosed with LCIS by biopsy develop invasive carcinomas at a frequency similar to that of women with untreated DCIS. • In patients observed for more than 20 years, invasive carcinoma develops in 25% to 35%. • However, unlike in DCIS, both breasts are at equal risk. • Invasive carcinomas developing in women after a diagnosis of LCIS are threefold more likely to be of lobular type compared with carcinomas overall, but the majority do not show specific lobular differentiation • regarded as marker of increased risk for both ipsilateral & contralateral breast = 10X • Frequently multifocal and bilateral (50 – 70%) • If untreated 30% develop carcinoma in either breast, lobular > ductal • If proliferation involves only portion of lobule = atypical lobular hyperplasia – 5X risk

Answer 10

5. Medullary • DCIS has been divided into five architectural subtypes: comedocarcinoma, solid, cribriform, papillary, and micropapillary • LCIS

Answer 11

WJI: I would suggest 1. is more false than 2. but could go either way. 2. Phyllodes tumour occurs in same age group as fibroadenoma - FALSE: *LW: Most present in 6th decade 10-20 yrs later than on average fibroadenoma presentation. Phyllodes mean age 45 years; younger in adenocarcinoma) Fine needle aspiration is inaccurate, and even core biopsy has moderate sensitivity due to tumour heterogeneity causing inadequate sampling.If < 2.5cm, probably fibroadenomaIf > 2.5

Answer 12

1. >3cm size. • Most are solitary and found in principal lactiferous ducts or sinuses, close to nipple • Rarely >1cm - 80% a/w unilateral serous or blood discharge

Answer 13

1. Cells are in pools of mucus • Colloid carcinomas are usually well circumscribed and may mimic benign lesions on physical examination and mammographically. • Neuroendocrine differentiation in the form of argyrophilic granules is present in 14% to 50%. • nodesmoplastic reaction, well circumscribed

Answer 14

• Precursors of invasive ductal carcinoma, especially comedocarcinoma • Underlying palpable mass in 50 – 60% - indicated invasive Ductal Ca • Histologic hallmark = involvement of epidermis by malignant cells (Paget cells) • Paget cells = large, with clear cytoplasm, and prominent nucleoli

Answer 15

3. Increased bilateral risk of ductal and lobular - T - probably best answer Contentious area. Has been thought LCIS is not a precursor to ILC, and is merely a risk factor for development of ipsilateral and contralateral invasive breast cancer (IDC > ILC). LCIS serves as a marker for increased risk for developing invasive carcinoma in either breast 10x. Some propose LCIS is a precursor. Argument that it can't be precursor as develop cancer in contralateral breast is thought maybe due to LCIS predilection for multifocal / bilateral distribution in the first instance - so can develop bilateral disease from the precursor lesions. Also, there is a skew of the bilateral invasive cancer to the ipsilateral LCIS breast side. Also finding E-cadherin problems in both LCIS and ILC.

Answer 16

Answer: Phyllodes tumours occur in the same age group as fibroadenoma (false)

Answer 17

4. MS - F - 1 per 1000 in USA and Europe. F>M 2x (1.4-2.3). Frequency increases with distance from equator. 7. Least common condition in females (taking this as a M vs F ratio, vs actual prevalence) (TW) 1. SLE - T - prevalence 1 in 200-500, incidence 104-170 per 100 000 women (USA). F>M 7-15x (adult), 3x (children), 8x (older adult). 2. Grave’s - T - incidence 1.5-2% of USA females. F>M 9x 3. Hashimoto’s - T - prevalence 0.55% of people. F>M 5x, and increases with age up to 20x more common in females. 4. MS - F - 1 per 1000 in USA and Europe. F>M 2x (1.4-2.3). Frequency increases with distance from equator. If taking question as 'least common condition' (ie prevalence / incidence) - ans probably 1 or 4.

Answer 18

*LW: based on repeat answers and details, i favour tubal peritoneal spread being most atypical **LJS - serous type: can exfoliate from endometrium, travel through tubal wall to implant on peritoneal surfaces. 20% type 1 endometrial ca has foci squamous differentiation ADB--> prob a bad recall path course notes say Type 2 endometrial cancer- serous type has a worse prognosis due to propensity for lymphatic and transtubal spread. keeping I mind that Type 2 serous makes up 15% of endometrial cancers. that doesn't seem too atypical. 4. If SCC then it is likely to be cervical carcinoma spreading to the uterus FALSE and hence it is the answer for this question 2. PATH2004 What is atypical in endometrial carcinoma ? 1. Focal mass 2. Diffuse thickening of uterus 3. Tubal to peritoneal spread serous type does this 4. If SCC then it is likely to be cervical carcinoma spreading to the uterus FALSE and hence it is the answer for this question

Answer 19

• Incorrect option not present • Endometrial polyps are sessile masses of variable size that project into the endometrial cavity (*LW: agree usually sessile masses) • Endometrial carcinoma - Localised polypoid tumour or diffuse tumour involving entire endometrial surface

Answer 20

• Tubular Carcinoma - Best differentiated of ductal carcinomas – best prognosis • Histologic subtypes. The 30-year survival of women with special types of invasive carcinomas (tubular, colloid, medullary, lobular, and papillary) is more than 60%, compared with less than 20% for women with cancers of no special type ("ductal carcinomas"). As discussed earlier, tubular and colloid carcinomas have an exceptionally good prognosis. [48] However, if the tumor is not "pure" in type, or poor prognostic factors are present such as large tumor size, poor nuclear grade, or lymph node involvement, the favorable prognosis may be diminished or eliminated.

Answer 21

**LJS - I would chose sclerosing adenosis Simple cysts rarely have rim calcification (much more common in oil cysts) *LW: Agree with above re option 4. sclerosing adenosis. Robbins: Ca++ usually associated with clusters of apocrine cysts, hyalinzed fibroadenoma, sclerosing adenonosis. No micro Ca++ in phyllodes. No mention of Ca++ in medullary carcinoma. STatDx: Curvilinear Ca++ with oils cysts / fat necrosis. 1 and 4 true• Calcifications are commonly found in cysts and adenosis and often form mammographically suspicious clusters • Sclerosing Adenosis commonly present as mammographic calcifications • Fibroadenoma – popcorn calcifications • Nothing mentiond about phyllodes or medullary having calcification • Cysts may have calcification

Answer 22

3. Ovarian thecoma

Answer 23

1. height above average - F - height tends to be below average 1. Sep03.06 Fragile X, false (TW) 1. height above average - F - height tends to be below average 2. mental retardation - T 3. mandible long - T - characteristic elongated face becomes apparent in later teen and adult years. Facial appearance is often described as long and narrow with prognathism and large ears. 4. hyperextensible lax joints - T - hyperflexible joints, flat feet, mitral valve prolapse occasionally occur. Fragile X is most common inherited cause of mental retardation. Caused by expansion of a repetition of the cytosine-guanine-guanine trinucleotide segment (CGG) of the fragile X mental retardation 1 (FMR-1) gene. Prevalence is 1 in 4000 males and 1 in 6000 females. UpToDate

Answer 24

*LW: According to the gospel of Donnelly: Congenital CNS infections = TORCH: Toxoplasmosis, other (Syphillis and HIV), rubella, CMV, and herpes. Congential herpes due to HSV 2, causing menigo enchaphlitis with cortical and white matter abnormalities, diffusion restriction, and meningeal enhancement. No predilection for location. Thus, I would favour chicken pox out of the provided answers, to be least correct. 8. Herpes - F - Both virus types 1 and 2 can cause genital infection and can be transmitted from mother to fetus or newborn. In utero infection is rare; 3% of these will have severe symptoms of skin vesicles/scarring, eye disease, microcephaphaly/hydranencephaly. HSV-2 is most commonly acquired during vaginal delivery (intrapartum), can also occur postnatally (horizontal transmission). Which of the following is not a congenital CNS infection: (GC) 4. Chicken pox Eric had this as the answer in 2004 Dahnert includes it in "Other", p232.? T - Congenital varicella syndrome occurs in 2% of children born to women who develop varicella during the 1st or 2nd trimester of pregnancy. Manifests as IUGR, cortical atrophy, microcephaly, microphthalmia, cataracts, limb hypoplasia, skin scarring. NB: Infantile zoster: maternal varicella infection after 20 wks gestation.Neonatal zoster: maternal infection within 5 days before or 2 days after delivery, fetus with acquire the virus transplacentally without any protective antibodies (insufficient time for Ab's to develop in the mother), results in severe & disseminated infection 5. Rubella T - Risk is high in the first trimester (90% before 11 wks gestation), then declines to 25% at 23-26 wks, and then rises to 67% after 31 wks. Infection in the first 11 wks is uniformly teratogenic however no birth defects occur in infants infected after 16 wks. Fetal infection occurs transplacentally during the maternal viraemic phase. Classic triad of congenital rubella syndrome: SNHL, ocular abnormalities, congenital heart disease. CNS abnormalities include mental retardation, encephalographic abnormalities, hypotonia, meningoencephalitis, and microcephaly. 6. CMV T - Most common congenital infection, can result from both primary and recurrent infections. One to 4% of women have a primary infection during pregnancy. 40% of these women transmit the virus to their fetus. 5-15% of the infants have signs of CMV disease. Congenital infection due to recurrent CMV is 0.5-1% and <1% of the infected infants have clinically apparent disease. Microcephaly, ventriculomegaly, cerebral atrophy, chorioretinitis, and SNHL. Periventricular calcifications, migrational anomalies if contracted in 1st trimester 7. Toxoplasmosis T - Vertical transmission, either in utero or during vaginal delivery. Approx. 30% of exposed fetuses acquire the infection, but most of the infants are asymptomatic. The severity of infection in the fetus depends on the gestational age at the time of transmission. In general, earlier infection is more severe but less frequent. As a consequence, 85% of live infants with congenital infection appear normal at birth. Very early infections (ie, occurring in the first trimester) may result in fetal death in utero or in a newborn with severe CNS involvement, such as cerebral calcifications, hydrocephalus, and chorioretinitis. 8. Herpes - F - Both virus types 1 and 2 can cause genital infection and can be transmitted from mother to fetus or newborn. In utero infection is rare; 3% of these will have severe symptoms of skin vesicles/scarring, eye disease, microcephaphaly/hydranencephaly. HSV-2 is most commonly acquired during vaginal delivery (intrapartum), can also occur postnatally (horizontal transmission). [eMedicine, Nelson textbook of pediatrics 17th ed., www.kcom.edu]

Answer 25

2. Hyperplasia can be difficult to differentiate from normal proliferative phase thickening F - US appearance can simulate that of normal thickening during the secretory phase; also sessile polyps, submucosal fibroids, cancer, adherent blood clots.Endometrial abnormality – incorrect: (GC) 1. Polyps are most commonly sessile T - rarely pedunculated. 2. Hyperplasia can be difficult to differentiate from normal proliferative phase thickening F - US appearance can simulate that of normal thickening during the secretory phase; also sessile polyps, submucosal fibroids, cancer, adherent blood clots. 3. Cancer may present with discrete mass T - may appear as a localised polypoid tumour 4. Cancer may present with diffuse endometrial thickening T - may appear as a diffuse tumour involving entire endometrial surface.

Answer 26

1. Best seen in proliferative phase T - imaging should be performed when the endometrium is thin: Proliferative phase = days 6-12, 5-7mm. Periovulatory phase = day 14, 11mm (trilaminar appearance). Secretory phase = days 15-28, 7-14mm. 24. Regarding endometrial polyps which is true: (GC) 1. Best seen in proliferative phase T - imaging should be performed when the endometrium is thin: Proliferative phase = days 6-12, 5-7mm. Periovulatory phase = day 14, 11mm (trilaminar appearance). Secretory phase = days 15-28, 7-14mm. 2. Differentiating benign submucosal fibroid and endometrial polyp by US is possible you generally can can’t you? SG F - best seen at sonohysterography, appear as echogenic, smooth,intracavitary cystic masses outlined by fluid. 3. Differentiation between fibroid and endometrial polyps possible on T2W F - Polyp: T2 hypointense intracavitary mass surrounded by high SI fluid and endometrium. Fibroid: T1 iso-hypo relative to myometrium, T2 homogeneously hypointense (may appear heterogeneously hyperintense when degeneration present), tend not to interrupt the endometrium unless submucosal (whereby they may distort the uterine cavity). 4. When associated with endometrial fluid as indication of malignancy F - Recognised cause of endometrial fluid. Other causes in a premenopausal woman include: infection, obstructive lesion (congenital/acquired), bleeding disorders, pregnancy (intrauterine, ectopic, incomplete abortion), endometrial cancer, submucosal fibroid, menstruation.

Answer 27

*LW: option 4 as least correct: Despite radiopedia stating increased colorectal cancer risk in BRCA 1, but NOT in BRCA2. Robbins states increased colon risk in BRCA1, but does not mention colon cancer increased in BRCA2 related text, however in table 23-3 mentions both BRCA1 and BRCA 2 have increased risk of colon cancer, and following page states " BRCA1 and BRCA 2 carriers also susceptible to other cancers such as colon, prostate and pancreas. if question 3 is talking about risk of breast cancer in those with a family Hx, then is correct with BRCA 1 and BRCA 2 fam Hx has a 60-80% risk of breast cancer. However, only approx 25% of familial breast cancers are attributed to BRCA mutations. **LJS - agree. Though my Robbins (big, 9th ed) table 23-3 does not list colorectal ca and neither does text. There are meta-analyses suggesting small incr risk of CRC in BRCA1 (but not BRCA2) but I would stick with Robbins answer https://pubmed.ncbi.nlm.nih.gov/30380096/ Previous answer: 4. Increased risk of colon cancer in BRCA1, but not BRCA2 - F - no, or very slightly increased in both. I have this as true in my notes (this is controversial - not in radiopedina) 12. BRCA 1, BRCA 2, which is least correct? (TW) 1. Both increase risk of ovarian cancer - T - both increase risk of ovarian cancer. 2. Increase risk of prostate cancer in both - T - both increase risk of prostate cancer 3. 50-70/80% in those with fam hx - T - Robbins table - BRCA1 has more than 70% risk of breast Ca by 80yo. BRCA2 has more than 60% risk by 70yo. 4. Increased risk of colon cancer in BRCA1, but not BRCA2 - F - no, or very slightly increased in both. I have this as true in my notes (SG)BRCA1 mutationbreast cancer: ~65%second primary breast cancer: ~30% at 5 yearsmale breast cancer: 1-2%ovarian cancer: ~32.5%prostate cancer: <30%pancreatic cancer: ~2%colorectal cancer: 5x increased risk if <50 years 4BRCA2 mutationbreast cancer: ~55%second primary breast cancer: ~10% at 5 yearsmale breast cancer: ~7.5%ovarian cancer: ~15%prostate cancer: <40%pancreatic cancer: ~5%colorectal cancer: no increased risk, or very slightly

Answer 28

1. Choriocarcinoma >5cm mass Choriocarcinoma- 5% of complete mole -> choriocarcinoma- 50% arise from complete mole- 25% from normal pregnancy- 25% from ectopic/miscarriage *RY - Repeat question - actually referring to testicular. In that instance, they are almost always <5cm.

Answer 29

*LW: quoting pathoma - metatases are the most important prognostic factor, although the vast majority present without mets, so hence next most important / most common prognostic fx is nodal stage. Quoting robbins: except for 10% who present with mets / inflammatory carcinoma, prognosis is determined by the pathologic examination of the primary carcinoma and axillary nodes. and Axillary nodal status is the most important prognostic fx for invasive carcinoma in absence of mets. Size of tumour second most important prognostic fx, and is indepedent from nodal stage. So I would favour A) presence or absence of distant mets as the most important prognostic fx. Followed next by nodal involvement. d. Nodal involvement and number of involved nodes T - single most important factor. 5YS with no nodes involved is close to 90%; with 16 or more nodes it drops to <50%. 12. Best prognostic factor in breast cancer: (GC) a. Distant metastases - those with haematogenous spread are rarely curable. b. Hormone receptor status, including HER2/neu - ER/PR positive status confers a slightly better prognosis, but reason for determining their presence is to predict response to therapy. Highest rate of response to anti-E2 therapy is seen in women with both ER and PR receptors; lower if only one of these present. Overexpression of HER2/neu is associated with a poor prognosis. c. Tumour grade and histologic subtype - all special types of Ca (tubular, medullary, mucinous, cribiform, adenoid cystic) have a better prognosis than NOS (latter <20% survival rate). d. Nodal involvement and number of involved nodes T - single most important factor. 5YS with no nodes involved is close to 90%; with 16 or more nodes it drops to <50%. e. Size of primary - <1cm have an excellent prognosis in the absence of LN mets, may not require chemotherapy. Added all options.

Answer 30

4. Serous cystadenocarcinoma T - frequently bilateral; complex cystic mass (non discriminatory), thick septae would favour malignancy; papillary projections often seen (and also suggest malignancy); psammoma bodies common. [CT/MR Imaging of Ovarian Tumours, RG 2002] 2. Bilateral ovarian cysts, internal septations, nodularity, calcifications: (GC) 1. Statistically mucinous cystadenocarcinoma most likely F - Overall, serous cystadenocarcinomas account for 50% of malignant ovarian tumours; whilst mucinous account for 10%. Serous tumours - 60% are benign, 15% borderline, 25% malignant. 65% bilateral.Mucinous tumours - 80% benign, 10% borderline, 10% malignant. 20% bilateral. 2. Morphologically serous and mucinous can’t be differentiated F - In terms of their pathologic features, disease course, and prognosis, serous and mucinous tumours are different. Clinical and imaging differentiation, however, is not easy. In many instances, epithelial tumours tend to be cystic and solid at gross examination, and their cell types cannot be differentiated on the basis of their appearance on MR/CT/US. That said, calcifications and papillary projections rare in mucinous tumours. 3. Calcification indicates psammoma bodies and therefore mucinous cystadenocarcinoma F - Calcifications in mucinous tumours tend to be linear (albeit rare). Psammoma bodies are seen in up to 30% of malignant serous tumours at histology. 4. Serous cystadenocarcinoma T - frequently bilateral; complex cystic mass (non discriminatory), thick septae would favour malignancy; papillary projections often seen (and also suggest malignancy); psammoma bodies common. [CT/MR Imaging of Ovarian Tumours, RG 2002]

Answer 31

1. Stage II **SCS; to go to stage 3 would need to invade to pelvic side wall or lower 1/3 of vagina For stage 4: rectum or bladder

Answer 32

3. Endometrial carcinosarcoma Carcinosarcomas are highly malignant biphasic tumours with both carcinomatous (epithelial) and sarcomatous (bone, cartilage, or skeletal muscle) components.

Answer 33

2. M and F normal, sister may be abnormal ? AR PCK?

Answer 34

1. CA 125 and endometrial carcinoma SCS: Ca125 useful for ovarian carcinoma primarily.

Answer 35

2. Subareola DCIS not easily identifiable on mammogram50% not detectable

Answer 36

1. Swimming in a pool of mucous - T - Colloid carcinoma is a round sticky tumor. Copious quantities of mucin are produced such that the neoplastic cells appear to float in a sea of mucoid material. *LW: Colloid tumour aka. mucinous carcinoma. 3. Colloid tumour of the breast is usually a rounded well defined lesion. Most likely because: 1. Swimming in a pool of mucous - T - Colloid carcinoma is a round sticky tumor. Copious quantities of mucin are produced such that the neoplastic cells appear to float in a sea of mucoid material. 2. Cells in indian file - F - this is evident in invasive lobular carcinoma 3. Signet ring cells – F - variant of infiltrating lobular Ca .Also seen in pleomorphic LCIS. 4. Intense lymphocytic infiltrate and no desmoplastic response - F - medullary carcinoma 5. If granulomas are present this implies can’t be infection or malignancy - F

Answer 37

3. Incidental – LCIS doesn’t calcify ?? *LW: LCIS is always an incidental finding in a biopsy performed for another reason as LCIS is NOT associated with calcification or stromal reactions that would form a density. *WJI -robbins says almost always incidental, no necrosis or calcifications, statdx says either occult or grouped amorphous calcifications on mammogram and florid LCIS subtype shows necrosis. I'd go Rob but ??

Answer 38

**SCS: Big Robbins. 9th ed. Pg 1054 “Approximately 12% of breast cancers occur due to inheritance of an identifiable susceptibility gene or genes” ADB--> big robins 10th ed pg 1047 refers to what AJL saying *AJL My Robbins states: "It is believed that one-quarter to one-third of breast cancers occur due to inheritance of a susceptibility gene or genes." and "Single gene mutations with moderate to high penetrance accounts for 8% to 17%" and "Mutations in BRCA1 and BRCA2 are responsible for 80% to 90% of single gene familial breast cancers and about 3% to 6% of all breast cancers." Therefore that would equate to 67-75% non-familial 2. 50-70%.... *LW: Robbins states only 13% of women with breast cancer have one affected relative, so... this would equal approximately 87%. 1. 90 - 95%

Answer 39

3. low grade lesions difficult to distinguish histologically from fibroadenoma ?? Robbins says similar but can be distinguished via mitoses etc *LW: nodal dissection not indicated as nodal mets is rare, and occur 10-20yrs older than fibroadenoma on average. *+SCS: Additional Robbins. -Only the stomal component metastasises. -The uncommon HG lesions give rise to haematogenous mets in 1/3 of cases -High Grade lesions may be difficult to distinguish from sarcomas. -“Low grade lesions RESEMBLE fibroadenomas but are more cellular and are mitotically active”

Answer 40

5. Neoplasm with precursor dividing into stromal and glandular tissue - F - benign tumor - new growth composed of both fibrous and glandular tissue. Multiple studies have shown that in some tumors, the fibrous (stromal) component is clonal and may hafe cytogenetic aberrations, but the epithelial component is polyclonal. Some believe fibroadenomas result from hyperplasia of normal lobular components rather than being a true neoplasm (WHO classification, J.N. Eble). 7. Fibroadenomas: 1. Increase in size with lactation and infarction - T - can cause increased size. Infarction may ultimately result in involution. 2. Usually less than 35 yrs - T - can occur at any age, but mean age 30yo, median age 25yo. Most common breast tumor under 25yo. 3. In patients on cyclosporin - T - almost half of women receiving cyclosporin A after renal Tx develop fibroadenomas. 4. Can develop into carcinomas rarely, usually complex fibroadenoma - T - risk of subsequent breast cancer is slightly elevated only if the fibroadenoma is complex, there is adjacent proliferative disease or a family history of breast cancer. For the majority of women with simple fibroadenomas, no increased risk of developing breast cancer. 5. Neoplasm with precursor dividing into stromal and glandular tissue - F - benign tumor - new growth composed of both fibrous and glandular tissue. Multiple studies have shown that in some tumors, the fibrous (stromal) component is clonal and may hafe cytogenetic aberrations, but the epithelial component is polyclonal. Some believe fibroadenomas result from hyperplasia of normal lobular components rather than being a true neoplasm (WHO classification, J.N. Eble).

Answer 41

3. MCDK - aka Potter type II. Sporadic non-familial disease secondary to abnormal metanephron differentiation. 1 in 4000 unilateral, 1 in 10,000 bilateral; increased incidence in infants of diabetic mums. Contralateral renal abnormality in 40%. US: large kidney with multiple cysts of variable size. Oligohydramnios would suggest bilateral MCDK or unilateral with contralateral renal agenesis. 7. 20 week fetus, multiple cysts, variable size and decreased liquor seen, maternal grandparent has some sort of polycystic kidney disease: (GC) 1. ARPKD - aka infantile PKD or Potter type I; 1 in 10,000. AR - PKHD1 gene on chromosome 6p, encodes fibrocystin. Perinatal type has renal disease >>> hepatic fibrosis. Onset of renal failure in utero - oligohydramnios - Potter's sequence. US: both kidneys enlarged and hyperechoic (unresolved 1-2mm cystic/ectatic dilatation of renal tubules increases the no. of acoustic interfaces), non-visualisation of urine in bladder, oligohydramnios in 1/3. 2. ADPKD - mean age at dx is 43yrs. Onset of cyst formation during first decade, cysts grow with age. May occur in utero/neonatal period, but rare. Again, cysts are small in kids so kidneys appear diffusely echogenic. 1 in 1000, PKD1 gene on 16p (and PKD2 gene on 4q). 3. MCDK - aka Potter type II. Sporadic non-familial disease secondary to abnormal metanephron differentiation. 1 in 4000 unilateral, 1 in 10,000 bilateral; increased incidence in infants of diabetic mums. Contralateral renal abnormality in 40%. US: large kidney with multiple cysts of variable size. Oligohydramnios would suggest bilateral MCDK or unilateral with contralateral renal agenesis. Not too sure on this one (SG)

Answer 42

15-30% have endometrial carcinoma or hyperplasia T - and is the most common malignant neoplasm arising from endometriosis (followed by clear cell Ca). 8. Ovarian endometrioid carcinoma, surprise diagnosis, see what on TVUS: (GC) a. 10% have cervical stenosis F b. 15-30% have endometrial carcinoma or hyperplasia T - and is the most common malignant neoplasm arising from endometriosis (followed by clear cell Ca). c. Bilateral involvement in 60% F - bilateral in 30-50% d. Cystic mass with calcification F - non specific imaging findings, typically a large complex cystic mass with solid components.

Answer 43

ovaries > uterine ligts > POD > uterine serosal surface > fallopian tubes > (recto)sigmoid > GU tract > ? laparotomy scars Ovaries 1 - 80% 9. Distribution of endometriosis, in which order: (GC) a. Ovaries 1 - 80% b. Chest 5 - Due to microembolisation (via lymphatics or vascular channels), perionteal-pleural migration (through diaphragmatic defects). Ost 5 yrs after pelvic endometriosis. Pleuritic chest pain, cyclic haemoptysis, catamenial pneumothorax (73%). c. Laparoscopic scar 4 d. Pouch of Douglas 2 e. GIT 3 - common on anterior wall of rectosigmoid; may also occur on distal ileum, caecum, appendix. ovaries > uterine ligts > POD > uterine serosal surface > fallopian tubes > (recto)sigmoid > GU tract > ? laparotomy scars Incidence: 10% of menstruating women; 15-25% of infertile women. 30-40% of women with endometriosis are infertile. [Dahnert; Robbins]

Answer 44

2. Downgrowth of endometrium T - Robbins: "growth of the basal layer of the endometrium down into the myometrium". Nests of endometrial stroma, glands, or both are found well down in the myometrium btn muscle bundles; may see continuity btn nests and overlying endometrium on a fortitutous section. Adenomyosis refers to a disorder in which endometrial glands and stroma are present within the uterine musculature (UpToDate). Downgrowth and invagination of basalis endometrium into myometrium with associated muscular hypertrophy (Top 100 gynae). The pathognomonic feature of adenomyosis is the presence of endometrial tissue within the myometrium at a distance of at least one low power field (some authorities insist on two low power fields) from the endomyometrial junction. The distance requirement is to preclude mistaking the normal endometrium between muscle fibers at the mucosa for adenomyosis when the specimen is transected for slide preparation

Answer 45

2. Complete mole T - Twinning with a complete mole and a fetus with a normal placenta has been reported. Cases of healthy infants in these circumstances have been reported. Women with coexistent molar and normal gestations are at higher risk for developing persistent disease and metastasis. Termination of pregnancy is a recommended option. **LJS - twinning with complete mole and normal fetus can occur. Ovarian theca lutein cysts are caused by elevated beta HCG and definitely more common in complete moles, but most sources (RP, stat dx, Prometheus) just list "gestational trophoblastic disease" as cause for theca lutein cysts, and there are plenty of papers stating it occurs occasionally/infrequently in partial moles. It all depends on HCG levels, which some sources say are elevated in partial mole, but not as high as complete, and other sources say is similar to normal pregnancy. Comes down to which is more common: twinning with complete mole or partial mole with significantly elevated HCG. RP says coincident complete mole is "extremely rare, estimated incidence is at ~1:10,000-100,000 gestations" I think the "keeping it simple" answer is partial mole. *AJL - I agree 11. Live 10 week pregnancy with cystic mass and bilateral ovarian cysts: (GC) 1. Choriocarcinoma in normal pregnancy F - 50% are preceded by a hydatidiform mole, 25% by an abortion, 3% by ectopic pregnancy, and the other 22% by a full-term pregnancy. ie. the more abnormal the conception, the greater the risk of developing choriocarcinoma. 2. Complete mole T - Twinning with a complete mole and a fetus with a normal placenta has been reported. Cases of healthy infants in these circumstances have been reported. Women with coexistent molar and normal gestations are at higher risk for developing persistent disease and metastasis. Termination of pregnancy is a recommended option. 3. Partial mole F - early embryogenesis occurs, fetus may be viable and is often growth restricted. Theca lutein cysts are absent (or extremely rare). **LJS - explanation includes overlap between both triploidy types - diandry (paternal = partial mole) and digyny (maternal = non-molar triploid pregnancy with severe IUGR and other abn but can survive briefly) 4. Metastatic choriocarcinoma F

Answer 46

3. Discharge / bloody T - Most cases are discovered by the appearance of a bloody, brownish discharge accompanied by a rising BhCG titre in blood and urine. [Robbins] 12. Presentation of choriocarcinoma, most likely: (GC) 1. Incidental finding on 1st obstetric scan F - 50% are preceded by a hydatidiform mole, 25% by an abortion, 3% by ectopic pregnancy, and the other 22% by a full-term pregnancy. 2. Hyperemesis F - symptoms of complete mole, due to very high BhCG 3. Discharge / bloody T - Most cases are discovered by the appearance of a bloody, brownish discharge accompanied by a rising BhCG titre in blood and urine. [Robbins] 4. Metastatic disease F - usually widespread haematogenous dissemination at time of diagnosis; most often to lungs (50%), vagina (30-40%), brain, liver, kidneys. However, most cases of gestational trophoblastic neoplasia are diagnosed when the serum hCG levels plateau or rise in patients being observed after the diagnosis of hydatidiform mole. If metastases are present, signs and symptoms associated with the metastatic disease, such as hemoptysis, abdominal pain, hematuria, and neurologic symptoms, may be present. [eMedicine]

Answer 47

1. Increased risk with increasing age T - incidence 1 in 232 in 4th decade, 1 in 29 in 7th decade. RR at age 80 is 1.45. 10. 85 yo female and breast cancer risks: (GC) 1. Increased risk with increasing age T - incidence 1 in 232 in 4th decade, 1 in 29 in 7th decade. RR at age 80 is 1.45. 2. Approaches incidence from mets (from other sources) 3. Risk of DCIS halves, but LCIS stays the same

Answer 48

3. Increased mortality with conservative therapy compared with mastectomy F - Although total (simple) mastectomy provides a "cure" rate of 98 -99% for the entire group, patients with localized DCIS are candidates for breast conserving therapy, with a similar likelihood of breast cancer-specific survival rates. Although the rate of local (in breast) recurrence is higher with breast conservation, survival following a local recurrence is excellent. Only 1/2 of all recurrences are invasive, and more than 80 % of invasive recurrences are potentially salvageable. 11. DCIS removed in 2003: (GC) 1. 10-20% DCIS risk T - recurrence post lumpectomy: low grade 0-10%, comedocarcinoma 40% 2. 1% die of disease T - 98% survival after 13 yrs 3. Increased mortality with conservative therapy compared with mastectomy F - Although total (simple) mastectomy provides a "cure" rate of 98 -99% for the entire group, patients with localized DCIS are candidates for breast conserving therapy, with a similar likelihood of breast cancer-specific survival rates. Although the rate of local (in breast) recurrence is higher with breast conservation, survival following a local recurrence is excellent. Only 1/2 of all recurrences are invasive, and more than 80 % of invasive recurrences are potentially salvageable. Treated DCIS — The natural history of treated DCIS can be best estimated from series of women undergoing lumpectomy rather than mastectomy for DCIS. Although the studies differ markedly in design, the following general conclusions can be drawn: - At 12-15 yrs follow-up, and regardless of histologic grade or use of radiation therapy, the majority do not recur locally. - Approximately 1/2 of all recurrences are invasive, regardless of the use of adjuvant therapy (ie, RT, tamoxifen). - Nearly all patients with a noninvasive recurrence and >90% of those with an invasive recurrence survive their disease after subsequent treatment, usually mastectomy [UTD] Treatment problems: [Dahnert] - occult invasion in 5-20% of patients - multifocality in 30% ( (=> 2 foci in same quadrant) - multicentricity (=> 1 focus in different quadrants with a minimum distance of 2cm) in 14% of lesions <25mm, and in 100% of lesions >50mm. - axillary mets (?) in 1-2%

Answer 49

1. Associated with BRCA 2 Wji: disagree. Tamoxifen is definite RF for endometrial cancer. brca is associated with ovarian cancers (breast, colorectal, prostate, ovary, pancreas)

Answer 50

**LJS - not sure why this is least important if changes from stage 1 to 2. I don't see involvement of the true pelvis anywhere in FIGO staging, and it seems pretty non-specific. Wouldn't the true pelvis always be involved given the location of the uterus? So I think this is least important https://radiopaedia.org/articles/endometrial-carcinoma?lang=gb **LW: as always agree, i wonder if this was to test and confuse with cervical FIGO stage 4, of extending beyond true pelvis? **LJS - further review: -Rectal involvement = stage 4 -Parametrial without side wall = 3B -True pelvis (descriptor is included in some texts (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4419423/) "Stage III represents tumor with local or regional spread beyond the uterus, but not outside the true pelvis" -External cervix involvement = changes from stage 1 to 2 So above answer unchanged - true pelvis always involved, involvement OUTSIDE true pelvis changes from stage 3 to 4 Previous answer 4. Involvement of myometrium versus external cervix - stage I versus stage II disease. Surgical staging allows for determination of disease extent and detection and/or resection of occult metastases. Staging can be safely performed at the time of hysterectomy without added morbidity, and provides proper guidance with respect to postoperative adjuvant therapy, avoiding needless radiation therapy in 85% of clinical stage I/II patients. Surgical staging includes routine TAH + BSO, with removal of all pelvic and paraaortic lymph nodes (at least to level of IMA).High-risk factors include depth of invasion >66%, grade 2 or 3 endometrioid adenoCa, LVI and older age (latter tend to get the serous type of ECa). [Oncodiagnosis panel RG 2006, Robbins]

Answer 51

1 is true 4. Regarding Adenomyosis, which is true: (GC) 1. Doesn’t cycle T - glands derive from the stratum basalis of the endometrium, hence don't undergo cyclical bleeding (unlike endometriosis). 2. Looks like a fibroid F - most commonly encountered lesion that resembles adenomyosis; differentiation is important as fibroid treated with myomyectomy, whereas adenomyosis requires hysterectomy.

Answer 52

1. Gastroschisis - F - generally not assoc with extra GIT abnormalities (unlike omphalocele). 5. Fetal hydrops associations: (TW) 1. Gastroschisis - F - generally not assoc with extra GIT abnormalities (unlike omphalocele). 2. Parvovirus - T - parvovirus B19 is cytotoxic to fetal blood cell precursors and may cause anemia and hydrops fetalis. 3. CDH - T - thoracic abnormalities assoc with hydrops fetalis: CCAM, CDH, pulmonary sequestration, chylothorax, lymphangiectasis, neoplasms, bronchogenic cyst. These lesions increase intrathoracic pressure and can obstruct venous return to the heart, leading to peripheral venous congestion (or can obstruct lymphatic duct). 4. Trisomy 18 - T - Aneuploidy is responsible for approx 10% of non-immune hydrops fetalis. Most common chromosomal cause of NIHF is monosomy X. Other aneuploidies are T21, T13, T18, T12, tetraploidy and triploidy, and rare deletions and duplications. Hydrops fetalis refers to presence of 2 or more of the following abnormal fetal fluid collections: ascites, pleural effusion, pericardial effusion, skin oedema, polyhydramnios. Major divisions Immune vs Nonimmune. Immune: red cell alloimmunization (eg, Rh(D), Kell). Non-immune: Genetic causes (aneuploidy / metabolic storage diseases); CVS (structures / arrhythmias / AV and venous malformations); Thoracic abnormalities; Anaemia; Infection diseases; GIT malformations; GUT malformations; Twin gestations.

Answer 53

2. Oesophageal atresia: 5% 1. Cardiac defect 30% FALSE - Approx 40% 2. Oesophageal atresia: 5% TRUE 3. Coarctation 20% Don’t think so

Answer 54

3. ALL *RY - Note for leukaemia a/w Downs syndrome: - ALL usually arises after 5 years - A megalokaryloblastic L usually arises before 5 years. (from pathoma).

Answer 55

FIGO system stage 0: carcinoma in situ stage I: limited to the body of the uterus Ia: no or less than half (≤ 50%) myometrial invasion Ib: invasion equal to or more than half (≥ 50%) of the myometrium stage II: cervical stromal involvement endocervical glandular involvement only is stage I stage III: local or regional spread of the tumor IIIa: tumor invades the serosa of the body of the uterus and/or adnexa IIIb: vaginal or parametrial involvement IIIc: pelvic or para-aortic lymphadenopathy stage IV: involvement of rectum and or bladder mucosa and or distant metastasis IVa: bladder or rectal mucosal involvement IVb: distant metastases, malignant ascites, peritoneal involvement

Answer 56

Revised FIGO staging of cervical carcinoma I: confined to cervix uteri IA: invasive carcinoma only diagnosed by microscopy IB: invasive carcinoma with measured deepest invasion ≥5 mm (greater than stage IA), lesion limited to the cervix uteri IIA: involvement limited to the upper 2/3rd of vagina without parametrial invasion IIB: with parametrial involvement but not up to the pelvic wall III: carcinoma involves the lower third of the vagina and/or extends to the pelvic wall and/or causes hydronephrosis or non‐functioning kidney and/or involves pelvic and/or paraaortic lymph nodes IIIA: carcinoma involves the lower third of the vagina, with no extension to the pelvic wall IIIB: extension to the pelvic wall and/or hydronephrosis or non‐functioning kidney (unless known to be due to another cause) IIIC: involvement of pelvic and/or paraaortic lymph nodes, irrespective of tumor size and extent IV: carcinoma has extended beyond the true pelvis or has involved (biopsy proven) the mucosa of the bladder or rectum (bullous edema, as such, does not permit a case to be allotted to stage IV) IVA: spread to adjacent organs IVB: spread to distant organs

path womens - formatted Flashcards

(80 cards)