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path womens - formatted Flashcards

1
Q
  1. 47.APRIL02 Which of the following statements concerning vaginal malignancy is LEAST correct?
  2. Most are squamous cell carcinomas
  3. Sarcoma botryoides occurs in the pediatric age group.
  4. In utero exposure to diethylstilbestrol increases the risk of later development of squamous cell carcinoma.
  5. Malignant involvement of the vagina is more likely as a result of spread from other genital tract malignancy, than as a primary tumour.
  6. Vaginal adenosis is a precursor lesion for adenocarcinoma.
A

Answer: In utero exposure to diethylstilbestrol increases the risk of later development of squamous cell carcinoma. (LEAST CORRECT

ROBBINS
Vaginal malignancy
- Virtually all primary carcinomas of the vain are Squamous cell carcinomas associated with high risk HPVs

Sarcoma Botryoides (grapelike)
- aka Embryonal Rhabdomyosarcoma
- uncommon vaginal tumor composed of malignant embryonal rhabdomyoblasts
- most frequently found in infants, children <5 yrs

Diethylstilbestrol
- used in 1940s-1960s to prevent threatened aborptions
- associated with mullerian duct anomalies (septate/double vagina, uterus didelphys)

Vaginal adenosis
- Small patches of residual glandular epithelium in the vagina which persists into adult life.
- associated with Diethylstilbestrol exposure in utero.
- rare cases of clear cell adenocarcinoma arising in the DES-related adenosis.

The most common malignant tumour to involve the vagina is carcinoma spreading from the cervix, followed by primary squamous cell carcinoma of the vagina.

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2
Q
  1. 48.APRIL02 Which of the following statements concerning the placenta is most correct
  2. Pre-eclampsia is thought to result from failure of conversion of the high-resistance spiral arteries of the decidua to low-resistance vascular sinuses.
  3. A circumvallate placenta carries a risk of resulting in vasa praevia.
  4. Twin-to-twin transfusion occurs only in monozygous pregnancies.
  5. Complete hydatidiform moles have a diploid genotype.
  6. Unlike choriocarcinoma of the ovary, choriocarcinoma of placental origin is poorly responsive to chemotherapy.
A
  1. Complete hydatidiform moles have a diploid genotype (robbins uses the word ‘pattern’ not genotype). (90% have 46,XX diploid pattern all derived from the sperm (a phenomenon called androgenesis). The remaining 10% are from the fertilization of an empty egg by two sperm (46,XX and 46,XY).)
  2. 48.APRIL02 Which of the following statements concerning the placenta is most correct
  3. Pre-eclampsia is thought to result from failure of conversion of the high-resistance spiral arteries of the decidua to low-resistance vascular sinuses. (Emedicine yes this is ? correct and is stated so in the Adelaide path notes and this web site, but ? more complex than this and therefore not the most correct)
  4. A circumvallate placenta carries a risk of resulting in vasa praevia. (circumvallate placenta = having an extrachorial part , premature labor, threatened abortion, increased perinatal mortality, marginal hemorrhage)
  5. Twin-to-twin transfusion occurs only in monozygous pregnancies. False – rarely can get dizygotic twins with communication between placentas
  6. Complete hydatidiform moles have a diploid genotype (robbins uses the word ‘pattern’ not genotype). (90% have 46,XX diploid pattern all derived from the sperm (a phenomenon called androgenesis). The remaining 10% are from the fertilization of an empty egg by two sperm (46,XX and 46,XY).)
  7. Unlike choriocarcinoma of the ovary, choriocarcinoma of placental origin is poorly responsive to chemotherapy. (Rapidly invasive, widely metastasised at Dx, but responds well to chemotherapy)
    • 90% have 46,XX diploid pattern, all derived from single sperm (phenomenon called androgenesis) – fertilisation of egg that has lost its chromosomes
    • 10% = fertilisation of empty egg by 2 sperm – may be 46,XX or 46,XY
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3
Q
  1. 44.APRIL02 A 40-year-old epileptic woman has a 24-week morphology obstetric ultrasound scan. In view of her age she had chorionic villus sampling at 11 weeks, which was normal. The scan shows choroid plexus cysts, clinodactyly, duodenal atresia, thickened nuchal skin fold and a complex cardiac septal defect. The most likely explanation of the chorionic villus sampling results is
  2. Sampling of necrotic placental tissue
  3. Confined placental mosaicism
  4. Fetal mosaicism
  5. Noonan Syndrome
  6. Phenytoin syndrome/ Fetal hydantoin syndrome
A
  1. Fetal mosaicism
  2. Sampling of necrotic placental tissue
  3. Confined placental mosaicism (Contrary to generalised mosaicism, which is characterised by the presence of two or more karyotypically different cell lines within both the fetus and its placenta, CPM represents tissue specific chromosomal mosaicism affecting the placenta only. The diagnosis of CPM is most commonly made when, after the diagnosis of chromosomal mosaicism in a CVS sample, the second prenatal testing (amniotic fluid culture or fetal blood culture analysis) shows a normal diploid karyotype.)
  4. Fetal mosaicism
  5. Noonan Syndrome (nuchal cystic hygroma, congenital heart disease, pleural effusions, normal karyotype)
  6. Phenytoin syndrome/ Fetal hydantoin syndrome (growth restriction,microcephaly, hypoplasia of the distal phalynx of the fingers and toes, nail hypoplasia, typical facial apperance with a low nasal bridge, hirsutism, cleft lip/palate, rib anomalies, and occasional cardiac and GU anomalies)
    • Approximately 1% of Down syndrome patients are mosaics, usually having a mixture of cells with 46 and 47 chromosomes.
    • This mosaicism results from mitotic nondisjunction of chromosome 21 during an early stage of embryogenesis. • Symptoms in such cases are variable and milder, depending on the proportion of abnormal cells.
    • Clearly, in cases of translocation or mosaic Down syndrome, maternal age is of no importance.
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4
Q
  1. 45.APRIL02 Which of the following statement concerning ovarian carcinoma is most correct?
  2. Germ cell tumours are the most common group of ovarian neoplasms.
  3. Mucinous cystadenomas are more likely to be bilateral than serous cystadenomas.
  4. The epithelial component of a serous cystadenocarcinoma resembles colon carcinoma.
  5. The Brenner tumour is the equivalent of the seminoma of the testis.
  6. Granulosa cell tumours commonly secrete oestrogen.
A
  1. Granulosa cell tumours commonly secrete oestrogen. (Produce large amounts of oestrogen with resultant precocious sexual development in young girls with functionally active tumours (juvenile granulose cell tumours) – 66% are in older women. Is a sex cord tumour)
  2. 45.APRIL02 Which of the following statement concerning ovarian carcinoma is most correct?
  3. Germ cell tumours are the most common group of ovarian neoplasms. (surface (coelomic) epithelium – 65-70%)
  4. Mucinous cystadenomas are more likely to be bilateral than serous cystadenomas. (serous - bilateral 25% , mucinous 5% bilateral)
  5. The epithelial component of a serous cystadenocarcinoma resembles colon carcinoma. (tubal like epithelium)
  6. The Brenner tumour is the equivalent of the seminoma of the testis. (Dysgerminoma - ovarian counterpart of seminoma of testis – sex cord tumour). Brenner tumour is a urothelial like tumour (surface epithelium derived).
  7. Granulosa cell tumours commonly secrete oestrogen. (Produce large amounts of oestrogen with resultant precocious sexual development in young girls with functionally active tumours (juvenile granulose cell tumours) – 66% are in older women. Is a sex cord tumour)
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5
Q
  1. 43.APRIL02 A 45-year-old woman is referred for MRI staging of cervical carcinoma. The tumour is limited to the pelvis. It replaces the cervix, does not extend into the parametriurn. It extends down the vagina only 2cm and there is a fat plane between the tumour and obturator internus, the rectum and bladder, These findings correspond to which-FIGO stage:
  2. Stage I b
  3. Stage II
  4. Stage lI S
  5. Stage Ill
  6. Stage I\/
A
  1. Stage II
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6
Q
  1. 39.APRIL02 All of the following conditions have an increased incidence in pregnacy/ postpartum period WITH THE EXCEPTION OF
  2. Disseminated intravascular coagulation
  3. Hashimoto’s
  4. Aortic dissection
  5. Pituitary insufficiency
  6. Fatty liver
A
  1. Hashimoto’s Thyrotoxicosis (thyroiditis but not thyrotoxicosis, Mark and Eric both agree on this but not 100% sp still poo brown)
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7
Q
  1. 19.03.65 PID which is NOT TRUE ? Rob p694
  2. 2 types – sexually transitted and peurperal
  3. Pueral is polymicrobial – Staph/Strep/Colitis
  4. Tubo-ovarian abscess sequence :hydrosalpinx – pyosalpinx – abscess
  5. Vaginal epith/endometrium relatively spared
  6. Gonoccoal inflammatory changes confined to mucosa/submucosa
A

*LW: per Robbins:
3. Tubo-ovarian abscess sequence :hydrosalpinx – pyosalpinx – abscess: FALSE:
Acute suppurative salpingitis:
Fimbrae may seal creating salpingo oophoritis.
Collections of pus within ovary in tube and ovary = tubo ovarian abscesses, or tubal lumen = pyosalpinx may occur.
With time; infecting organism may disappear, pus undergoing proteolysis to a thin serous fluid producing hydrosalpinx or hydrosalpinx follicularis.

19.03.65 PID which is NOT TRUE ? Rob p694
  1. 2 types – sexually transmitted and peurperal (puerperal and STD group classification): TRUE
  2. Puerperal is polymicrobial – Staph/Strep/Colitis (Staph, Strep, coliforms, C. perfringens): TRUE
  3. Tubo-ovarian abscess sequence :hydrosalpinx – pyosalpinx – abscess FALSE: Acute suppurative salpingitis:
    Fimbrae may seal creating salpingo oophoritis.
    Collections of pus within ovary in tube and ovary = tubo ovarian abscesses, or tubal lumen = pyosalpinx may occur.
    With time; infecting organism may disappear, pus undergoing proteolysis to a thin serous fluid producing hydrosalpinx or hydrosalpinx follicularis.
  4. Vaginal epith/endometrium relatively spared (Vagina and endometrium usually spared)
  5. Gonoccocal inflammatory changes confined to mucosa/submucosa (acute suppurative reaction confined to mucosa and submucosa): TRUE
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8
Q
  1. 19.03.66 Carcinoma of cervix ? Rob p686
  2. CIN III progress to invasive in <1%
  3. 95% are squamous
  4. recognised types are polypoid, fungating, ulcerating, multifocal ands sessile
  5. prognosis is good even for stage IV disease (5 years survival 40-75%)
  6. Involvement of lower 1/3 vagina, bladder or bowel is Stage III
A
  1. 95% are squamous 8. 19.03.66 Carcinoma of cervix ? Rob p686
  2. CIN III progress to invasive in <1% (high likelihood of spreading)
  3. 95% are squamous
  4. recognised types are polypoid, fungating, ulcerating, multifocal ands sessile (fungating (most common), ulcerating or infiltrative)
  5. prognosis is good even for stage IV disease (5 years survival 40-75%) (10%)
  6. Involvement of lower 1/3 vagina, bladder or bowel is Stage III (bladder and bowel stage IV)
    • Squamous cell carcinoma (SCC) accounts for 80-90% of all cervical malignancies
    • 95% of squamous carcinomas are composed of large cells, either keratinising (well differentiated) or non-keratinising (moderately differentiated)
    • Invasive cervical carcinoma can be o fungating (most common)
    o ulcerating
    o infiltrative  
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9
Q
  1. 19.03.67 Carcinoma of the endometrium risk factor include following EXCEPT ? Rob p691
  2. HT
  3. DM
  4. Obesity
  5. Long term stimulation with progrestone
  6. Infertity
A

*LW:
4. Long term stimulation with progrestone: FALSE, correct risk factor is unopposed oestrogen.

• Risk Factors / Associations
o polycystic ovaries (Stein-Leventhal Syndrome)
o feminizing ovarian neoplasms → Granulosa-theca cell: oestrogen secreting
o late menopause
o hormone replacement Rx
o Obesity
o Diabetes (60% have abnormal glucose tolerance)
o Hypertension
o Infertility - single and nulliparous women with Hx suggestive of functional menstrual irregularities consistent with anovulatory cycle

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10
Q
  1. 19.03.68 48 year old female with marked increase in endometrial thickness and 5cm solid mass on ovary. LIKELY cause is ?
  2. Ectopic Preganacy
  3. Metastatic endometrial cancer
  4. Ovarian Thecoma
  5. Endometrial cancer
A
  1. Ovarian Thecoma (Granulosa-Theca Cell Tumors more common to cause endometrial thickening)

• Conditions leading to hyperplasia include
o polycystic ovarian disease (Stein-Leventhal syndrome)
o functioning granulosa cell tumors of the ovary

• In adults, a/w endometrial hyperplasia/carcinoma and cystic disease of the breast
o excessive cortical function (cortical stroma hyperplasia)
o estrogen replacement therapy
o These are the same influences postulated to be of pathogenetic significance in a portion of endometrial carcinomas, discussed later.

• Pure thecomas are solid, firm tumours
o Most tumours are hormonally inactive but predominantly thecomas may be active

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11
Q
  1. 19.03.69 Which is a surface epithelial tumour of the ovary ? Rob p695
  2. Teratoma
  3. Dysgerminoma
  4. Endometriod Carcinoma
  5. Sertoli Cell tumour
  6. Yolk sac tumour
A
  1. Endometriod Carcinoma 11. 19.03.69 Which is a surface epithelial tumour of the ovary ? Rob p695
  2. Teratoma (Germ Cell)
  3. Dysgerminoma (Germ Cell)
  4. Endometriod Carcinoma
  5. Sertoli Cell tumour (Sex Cord Stroma)
  6. Yolk sac tumour (Germ Cell)
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12
Q
  1. 19.03.70 INCIDENCE of ectopic pregnancy is ? Rob p701
  2. 1 in 100-150
  3. 1 in 300
  4. 1 in 1500
  5. 1 in 3000
  6. 1 in 7000
A
  1. 1 in 100-150

• 1 in 150 pregnancies
• 1% of diagnosed pregnancies

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13
Q
  1. 19.03.71 Karyotype of classic mole (?complete mole)) is ? Rob p702
  2. 46 XX or XY chromosomes only paternal
  3. 46 CC- XY Y chromosome only paternal
  4. 46 XX – all chromosomes paternal
  5. 69 XXX, XXY or XYY
  6. 46,69 XXY
A

Answer: 46 XX or XY chromosomes only paternal

Complete mole - 2 types.

Homozygous complete mole
- single sperm (23X) + empty ovum = chromosome duplication
- 46XX

Heterozygous complete mole
- Dispermy (23X or Y) + empty ovum
- 46XX or 46XY

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14
Q
  1. Sep03.14 Which of the following is not a sex cord/stromal tumour?
  2. Yolk sac
  3. Granulosa theca
  4. lutein cell
  5. Sertoli Leydig cell
A
  1. Yolk sac (germ cell tumour)

Sex cord- stromal tumors
• Granulosa-stromal cell tumors
o Granulosa cell tumors
o Tumors of the thecoma-fibroma group
• Sertoli-stromal cell tumors; androblastomas
• Sex cord tumor with annular tubules
• Gynandroblastoma
• Steroid (lipid) cell tumors

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15
Q
  1. Sep03.21 Female, primary amenorrhoea, short stature. Pelvic ultrasound - no ovaries seen. What is the most likely diagnosis?
  2. female pseudohermaphodism
  3. turners syndrome
A
  1. turners syndrome Turners

• Results from complete or partial monosomy of the X chromosome and is characterised primarily by hypogonadism in phenotypic females.
• Single most important cause of primary amenorrhoea
• Short stature
• Low posterior hairline, webbed neck
• Coarctation of the aorta
• Ovaries are reduced to atrophic fibrous strands, devoid of ova and follicles (streak ovaries) Female Pseudohermaphroditism
• XX. Development of ovaries and internal genitalia normal
• Excessive androgenic hormones in early gestation

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16
Q
  1. Sep03.33 38 year old with bilateral enlarged ovaries and marked endometrial thickening. Cause ?
  2. Polycystic ovaries
  3. Granulosa – theca cell ovarian tumour
  4. Endometrial carcinoma & bilateral ovarian metastases
A
  1. Polycystic ovaries (Ovaries twice normal size (> 15 cm3))
  2. Sep03.33 38 year old with bilateral enlarged ovaries and marked endometrial thickening. Cause ?
  3. Polycystic ovaries (Ovaries twice normal size (> 15 cm3))
  4. Granulosa – theca cell ovarian tumour (Unilateral)
  5. Endometrial carcinoma & bilateral ovarian metastases (not usually mets, can be synchronous tumours)
    • Granulosa – theca cell ovarian tumour- Unilateral
    • Polycystic ovaries - Ovaries twice normal size (> 15 cm3)
    • Conditions leading to hyperplasia include
    o polycystic ovarian disease (Stein-Leventhal syndrome)
    o functioning granulosa cell tumors of the ovary
    • In adults, a/w endometrial hyperplasia/carcinoma and cystic disease of the breast
    o excessive cortical function (cortical stroma hyperplasia)
    o estrogen replacement therapy
    o These are the same influences postulated to be of pathogenetic significance in a portion of endometrial carcinomas, discussed later.
    • Endometroid Tumours
    o 20% ovarian of cancers
    o 40% are bilateral
    o 15% associated with endometrial cancer (synchronous not mets)
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17
Q
  1. Sep03.34 What is atypical in endometrial carcinoma ?
  2. Focal mass
  3. Diffuse thickening of uterus
  4. Tubal to peritoneal spread
  5. If SCC then it is likely to be cervical carcinoma spreading to the uterus
A

*LW:
Difficult question, which is repeated in RD section:
I favour that tubal to peritoneal spread is more atypical, as although does occur, it occurs less frequently (as superficial papillary subtype is rare) than endometrial CA having Squamous components (metaplasia not frank SCC), and compared to the relatively common SCC of the cervix spreading to involve the endocervix uteri…..
*RY - I wonder if this question was referring to endometroid (type 1) endometrial cancer, in which case 3 would definitely be false, not just based on likelihood…? Up to 20% type 1 endometrial cancer contain foci of squamous differentiation.

  1. If SCC then it is likely to be cervical carcinoma spreading to the uterus
  2. Sep03.34 What is atypical in endometrial carcinoma ?
  3. Focal mass (localized polypoid tumor or as a diffuse tumor involving the entire endometrial surface)
  4. Diffuse thickening of uterus
  5. Tubal to peritoneal spread (papillary serous carcinoma, relatively superficial endometrial involvement may be associated with extensive peritoneal disease, suggesting spread by routes)
  6. If SCC then it is likely to be cervical carcinoma spreading to the uterus
    • In gross appearance, endometrial carcinoma presents either as a localized polypoid tumor or as a diffuse tumor involving the entire endometrial surface
    • Spread generally occurs by direct myometrial invasion with eventual spread to the periuterine structures by direct continuity.
    • Spread into the broad ligaments may create a clinically palpable mass.
    • Dissemination to the regional lymph nodes eventually occurs, and in the late stages, the tumor may be hematogenously borne to the lungs, liver, bones, and other organs.
    • In certain types, specifically papillary serous carcinoma, relatively superficial endometrial involvement may be associated with extensive peritoneal disease, suggesting spread by routes (i.e., tubal or lymphatic transmission) other than direct invasion.
    • 2 – 20% contain foci of squamous differentiation – usually benign (= adenocarcinoma with squamous metaplasia, or adenoacanthoma)
    • Moderately or poorly differentiated endometrioid carcinomas contain frankly malignant squamous elements (= adenosquamous carcinomas if > 10% tumour is squamous)
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18
Q
  1. Sep03.45 Who is at the greatest risk for hydatiform mole
  2. Israel
  3. Sweden
  4. New Zealand
  5. US
  6. Indonesia
A
  1. Indonesia 10/1000 (vs 1/1000 in USA)
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19
Q
  1. Sep03.XX Diagnosis of trophoblastic disease is dependent on
  2. curettage
  3. histopathology absence of syncitiotrophoblasts
A
  1. curettage
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20
Q
  1. 19.03.80 Patient with elevated CA 125 ? Rob p695
  2. Colon cancer
  3. Ovarian cancer
  4. Any ovarian pathology
  5. Adenocarcinoma
A

*LW:
Although most commonly associated with ovarian epithelial neoplasms, given it is also associated with non gynae malignancies (e.g. colon), I would favour in complete recall as….
1. Colon cancer: possibly elevated
2. Ovarian cancer: usually elevated in moderate - advanced disease
3. Any ovarian pathology: true
4. Adenocarcinoma: vague but possible as would assume adenocarcinoma of colon / breast / endometrium could possibly secrete Ca-125.

  1. Any ovarian pathology
    • CA 125 is a marker for serous carcinoma, esp carcinoma of the ovary, but elevations are also seen in peritoneal disease of any cause
    • CA-125 test results can be elevated by pregnancy, liver disease, endometriosis, fibroid tumors of the uterus, and diverticulitis, to mention a few of the non-cancerous conditions. It may also be high in patients with cases of cancers of the breast, lung, colon and pancreas.
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21
Q
  1. 19.02.29 On FNA of right ovarian mass transitional cells are found. Likely diagnosis is? Rob p695
  2. Brenner tumour
  3. Cyst adenocarcinoma
  4. Mucinous carcinoma
  5. Dermoid
  6. Leydig-Sertoli tumour
A
  1. Brenner tumour (epithelial components consist of nests of transitional cells resembling epithelium of urinary tract)
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22
Q
  1. 19.02.58 Patient with BRCA1 and known Ca breast aged 70yrs. Risks of Ca Ovary and type are ? Rob p695 big Rob p1067
  2. 4-9% No particular type
  3. 15-20% Cystadenocarcinoma
  4. Various risks and subtypes
A
  1. 15-20% Cystadenocarcinoma (Commonly serous cystadenomcarcima)

WJI: BRCA1 40% lifetime risk ovarian cancer, BRCA2 11-17%

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23
Q
  1. 19.02.44 Regarding cervical carcinoma ? Rob p688
  2. Carcinosarcoma is an atypical form
  3. CIN III has koilocytes
  4. CIN I is like condyloma accuminata
A

***LW: agree with LJS, in that CIN III loses koilocytes, and hence FALSE.
—> The squamous intraepithelial lesions of the cervix are divided into low-grade and high-grade lesions. The cytological hallmark of an LSIL is the koilocyte (‘hollow cell’) (Figure 15). Koilocytes are mature squamous cells with recognizable nuclear and cytoplasmic alterations. They derive their characteristic morphology in large part because of productive HPV infection.
—> The morphological changes seen in HSILs are similar to but distinct from those of LSIL. HSIL cells have a high nuclear–cytoplasmic volume ratio, greater nuclear hyperchromasia, complex nuclear membrane irregularities, and marked variation in nuclear size. In contrast to koilocytes, the stigmata of a productive HPV infection (binucleation and cytoplasmic cavitation) are not seen.

Cracinosarcoma:
–> Carcinosarcomas are tumors with both malignant epithelial and malignant mesenchymal components. They are relatively common in uterine corpus but extremely rare in cervix, with only approximately 62 cases reported in cervix in the English literature.

So out of listed options, I would favor option 3, CIN I is like condyloma accuminata

*AJL - I would favour 2. CIN III has koilocytes.
The typical changes to cells in squamous intraepithelial neoplasm (previously CIN) is a koilocyte and is seen with both LSIL and HSIL.
CIN III (and CIN II) is now called HSIL. CIN I is called LSIL.

**LJS - I thought CIN3 lost koilocytic change

Previous answer:
3. CIN I is like condyloma accuminata (CIN 1 is indistinguishable histologically from condylomata acuminata)

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24
Q
  1. 19.02.68 Pseudomyxoma peritoneii in perimenopausal female best explained by ? Big Rob p1070
  2. Ovarian mucinous cystadenocarcinoma
  3. Ca Stomach
  4. Mucocoele of appendix and rupture
A

*LW: agrees with below answer, with Robbins stating that technically pseudomyoxoma peritoneii is mucocele of appendix with rupture, which also commonly has bilateral ovarian deposits.
Option 3:

  1. Mucocoele of appendix and rupture this is correct according to Robbins (SOUNDS GOOD)Pseudomyxoma peritoneii is associated with a tumour – either appendiceal or ovarian mucinous adenocarcinoma. It requires not just mucus to be released into the peritoneum but also peritoneal implants of malignant tissue with cellular proliferation to get this (Big R p840 6th Ed.). Robbins states this clearly. B&H does muddy the water by saying that a mucocele can cause pseudomyxoma peritonei. Instances in which pseudomyxoma peritonei is accompanied by both appendical and ovarian mucinous adenocarcinomas are usually ascribed to spread by an appendiceal lesion Big Rob p840
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25
Q
  1. 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
  2. Trophoblast margin sampled
  3. Mosaicism confined to the placenta
  4. Trisomy 7 has bowel and palatal defects not visible on US
  5. Trisomy 7 associated with hydrops and fetal death in third trimester
A
  1. 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.

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26
Q
  1. 42.APRIL02 Which of the following statements concerning invasive breast carcinoma is most correct?
  2. “Indian-filing” of neoplastic cells is a classical histological feature of medullary carcinoma
  3. Bilateral tumours are most likely to occur with colloid carcinomas.
  4. Tubular carcinoma commonly incites a prominent desmoplastic response.
  5. Invasive lobular carcinoma accounts for about 30% of invasive breast carcinoma.
  6. Monoclonal proliferation of epithelial and myoepithelial cells is a feature of invasive ductal carcinoma.
A
  1. Tubular carcinoma commonly incites a prominent desmoplastic response. (Desmoplastic stroma prominent)
  2. 42.APRIL02 Which of the following statements concerning invasive breast carcinoma is most correct?
  3. “Indian-filing” of neoplastic cells is a classical histological feature of medullary carcinoma.(invasive lobular carcinoma)
  4. Bilateral tumours are most likely to occur with colloid carcinomas. (invasive lobular carcinoma)
  5. Tubular carcinoma commonly incites a prominent desmoplastic response. (Desmoplastic stroma prominent)
  6. Invasive lobular carcinoma accounts for about 30% of invasive breast carcinoma. (5-10%)
  7. 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)
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27
Q
  1. 34.APRIL02 Which of the following statement is LEAST correct concerning breast cancer prognosis?
  2. Invasion through the lymph node capsule indicates a poorer prognosis than simple node involvement alone
  3. If there is no lymph node involvement 10 year survival rates are 70 to 80%
  4. If the breast cancer is smaller than 1 cm there is a greater than 95% year survival.
  5. As a group, colloid carcinomas have a poorer prognosis than ductal carcinoma of no special type
  6. Tumours of poor grade have a significantly worse prognosis than tumours of high grade
A
  1. 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”))
  2. 34.APRIL02 Which of the following statement is LEAST correct concerning breast cancer prognosis?
  3. 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)
  4. 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
  5. If the breast cancer is smaller than 1 cm there is a greater than 95% year survival. (if <2cm 96% 5 YS)
  6. 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”))
  7. Tumours of poor grade have a significantly worse prognosis than tumours of high grade (87% grade I vs 13% grade III)
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28
Q
  1. Sep03.32 Breast cancer – lobular carcinoma is poorly seen. Why ?
  2. surrounded by inflammatory cells which blur the margins
  3. Diffuse Growth In Characteristic ‘Indian File’
A

• Diffuse Growth In Characteristic ‘Indian File’

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29
Q
  1. Sep03.12 Papillary type is not found in :
  2. invasive ductal breast Ca
  3. bladder Ca
  4. thyroid Ca
  5. RCC
  6. Breast
  7. Craniopharyngioma
A

• 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)

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30
Q
  1. 46.APRIL02 A 45-year-old woman has a breast ultrasound, which finds a suspected 2 cm carcinoma with enlarged abnormal mobile axillary nodes. These findings were confirmed with fine needle aspiration. Formal work up shows no disease elsewhere. What stage is this cancer?
  2. Stage I
  3. Stage II
  4. Stage Ill
  5. Stage IV
  6. The supplied information is insufficient for staging.
A
  1. 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)

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31
Q
  1. 19.03.75 Breast cancer – which type has WORST prognosis ? Rob p710
  2. Lobular
  3. Ductal – NOS
  4. Medullary
  5. Tubular
  6. Papillary
  7. DCIS
  8. Mucinous
A
  1. 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

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32
Q
  1. 19.03.72 Sclerosing adenosis which is NOT TRUE ? Rob p707
  2. Usually presents with calcification on mammogram
  3. May present as hard palpable mass
  4. Distinguished from cancer as does not cause compression and distortion of acni
  5. Slight increased cancer risk
A
  1. 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
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33
Q
  1. 19.03.73 LCIS which is MOST TRUE ? Rob p710
  2. Develop lobular carcinoma at same site
  3. Increase risk of lobular bilateral
  4. Increase risk of ductal and lobular
A
  1. 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

34
Q
  1. Sep03.61 Types of ductal carcinoma-in-situ: which is NOT?
  2. Cribriform
  3. Papillary
  4. Micropapillary
  5. Comedocarcinoma
  6. Medullary
A
  1. Medullary
    • DCIS has been divided into five architectural subtypes: comedocarcinoma, solid, cribriform, papillary, and micropapillary
    • LCIS
35
Q
  1. 19.03.74 Regarding breast which is FALSE Rob p710
  2. Fibroadenomas associated with increased risk of cancer
  3. Phyllodes tumour occurs in same age group as fibroadenoma
  4. Fibroadenoma occur in patient on cyclosporin
  5. Polyclonal or monoclonal proliferations
A

WJI: I would suggest 1. is more false than 2. but could go either way.

  1. 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

36
Q
  1. Sep03.13 Ductal papilloma of the breast. Which is the least correct?
  2. > 3cm size.
  3. Central location
  4. Associated with bleeding
A
  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
37
Q
  1. 25.02.40 Colloid carcinoma round and well-defined on mammo because ? Rob p1111
  2. Cells are in pools of mucus
  3. Abnormality is encapsulated
A
  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
38
Q
  1. 25.02.41 With Paget’s disease of the nipple, there is no mammographic abnormality because ? Rob p1107
  2. Abnormality distal to……..and in areola
  3. More commonly associated with lobular carcinoma
    3.
A

• 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  

39
Q
  1. LCIS, which is true
  2. Develop lobular carcinoma at same site
  3. Increased risk of lobular carcinoma bilateral
  4. Increased bilateral risk of ductal and lobular
A
  1. 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.
40
Q
  1. Regarding breast which is FALSE
  2. Fibroadenoma associated with increased risk of cancer
  3. Phyllodes tumour occurs in same age group as fibroadenoma
  4. Fibroadenoma occur in patient on cyclosporine
  5. Polyclonal or monoclonal proliferations
A

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

41
Q
  1. Least common condition in females
  2. SLE
  3. Grave’s
  4. Hashimoto’s
  5. MS
A
  1. MS - F - 1 per 1000 in USA and Europe. F>M 2x (1.4-2.3). Frequency increases with distance from equator.
  2. Least common condition in females (taking this as a M vs F ratio, vs actual prevalence) (TW)
  3. 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).
  4. Grave’s - T - incidence 1.5-2% of USA females. F>M 9x
  5. Hashimoto’s - T - prevalence 0.55% of people. F>M 5x, and increases with age up to 20x more common in females.
  6. 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.
42
Q
  1. PATH2004 What is atypical in endometrial carcinoma ?
  2. Focal mass
  3. Diffuse thickening of uterus
  4. Tubal to peritoneal spread
  5. If SCC then it is likely to be cervical carcinoma spreading to the uterus
A

*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.

  1. 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 ?
  3. Focal mass
  4. Diffuse thickening of uterus
  5. Tubal to peritoneal spread serous type does this
  6. If SCC then it is likely to be cervical carcinoma spreading to the uterus FALSE and hence it is the answer for this question
43
Q
  1. PATH2004 Endometrial abnormality – incorrect
  2. Polyps most commonly sessile
  3. Cancer may present with discrete mass
  4. Cancer may present with diffuse endometrial thickening
A

• 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

44
Q
  1. PATH2004 Breast cancer – which type has BEST prognosis / histological prognostic factors for breast cancer ?
A

• 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.

45
Q
  1. PATH2004 Regarding Ca2+ which is true
  2. Breast cysts have curvilinear Ca2+
  3. MicroCa2+ + phyllodes
  4. MicroCa2+ and medullary Ca
  5. Sclerosing adenosis
A

**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

46
Q
  1. 48y F with increased endometrial thickness and 5 mm solid mass on ovary likely cause is:
  2. Ectopic pregnancy
  3. Metastatic endometrial carcinoma
  4. Ovarian thecoma
  5. Endometrial carcinoma
A
  1. Ovarian thecoma
47
Q
  1. Sep03.06 Fragile X, false:
  2. height above average
  3. mental retardation
  4. mandible long
  5. hyperextensible lax joints
A
  1. height above average - F - height tends to be below average
  2. Sep03.06 Fragile X, false (TW)
  3. height above average - F - height tends to be below average
  4. mental retardation - T
  5. 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.
  6. 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
48
Q

Which of the following is not a congenital CNS infection:

  1. Chicken pox
  2. Rubella
  3. CMV
  4. Toxoplasmosis
  5. Herpes
A

*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.

  1. 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]

49
Q

Endometrial abnormality, which is incorrect:

  1. Polyps are most commonly sessile
  2. Hyperplasia can be difficult to differentiate from normal proliferative phase thickening
  3. Cancer may present with discrete mass
  4. Cancer may present with diffuse endometrial thickening
A
  1. 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)
  2. Polyps are most commonly sessile T - rarely pedunculated.
  3. 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.
  4. Cancer may present with discrete mass T - may appear as a localised polypoid tumour
  5. Cancer may present with diffuse endometrial thickening T - may appear as a diffuse tumour involving entire endometrial surface.
50
Q
  1. Regarding endometrial polyps which is true
  2. Best seen in proliferative phase
  3. Differentiating benign submucosal fibroid and endometrial polyp by US is possible
  4. Differentiation between fibroid and endometrial polyps possible on T2W
  5. When associated with endometrial fluid as indication of malignancy
A
  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. Regarding endometrial polyps which is true: (GC)
  3. 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.
  4. 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.
  5. 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).
  6. 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.
51
Q
  1. BRCA 1, BRCA 2, which is least correct?:
  2. Both increase risk of ovarian cancer
  3. Increase risk of prostate cancer in both
  4. 50-70/80% in those with fam hx
  5. Increased of colon cancer in BRCA1 but not BRCA2
A

*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)

  1. BRCA 1, BRCA 2, which is least correct? (TW)
  2. Both increase risk of ovarian cancer - T - both increase risk of ovarian cancer.
  3. Increase risk of prostate cancer in both - T - both increase risk of prostate cancer
  4. 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.
  5. 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
52
Q
  1. With regards to germ cell tumours, which is false?
  2. Choriocarcinoma >5cm mass
A
  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.

53
Q
  1. Best prognostic factor in breast cancer:

a. Distant metastases
b. Hormone receptor status, including HER2/neu
c. Tumour grade and histologic subtype
d. Nodal involvement and number of involved nodes
e. Size of primary

A

*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%.

  1. 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.
54
Q
  1. Bilateral ovarian cysts, internal septations, nodularity, calcifications:
  2. Statistically mucinous cystadenocarcinoma most likely
  3. Morphologically serous and mucinous can’t be differentiated
  4. Calcification indicates psammoma bodies and therefore mucinous cystadenocarcinoma
  5. Serous cystadenocarcinoma
A
  1. 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)
  3. 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.
  4. 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.
  5. 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.
  6. 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]
55
Q
  1. Hematometra with cervical lesion involving upper vagina
  2. Stage II
  3. Stage III
  4. Vaginal primary
A
  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

56
Q
  1. Thickened endometrial mass shows areas of osteoid, cartilage and muscle on biopsy. Most likely
  2. Hamartoma
  3. Metastatic immature teratoma
  4. Endometrial carcinosarcoma
A
  1. Endometrial carcinosarcoma Carcinosarcomas are highly malignant biphasic tumours with both carcinomatous (epithelial) and sarcomatous (bone, cartilage, or skeletal muscle) components.
57
Q
  1. Newborn with multiple small renal cysts. Mother father and sister are to be imaged. Which is the most likely?
  2. Mother, father and sister have normal imaging
  3. M and F normal, sister may be abnormal
  4. Sibling may have it
  5. Both parents may have it
A
  1. M and F normal, sister may be abnormal ? AR PCK?
58
Q
  1. Which serological markers are not useful:
  2. CA 125 and endometrial carcinoma
  3. Alfa fetoprotein in cirrhosis
  4. Calcitonin in thyroid mass
  5. BHCG in gynae tumour
A
  1. CA 125 and endometrial carcinoma

SCS: Ca125 useful for ovarian carcinoma primarily.

59
Q
  1. Pagets of the nipple - reasons why you can’t see it on mammo
  2. Involves skin of areola and rarely extends further back than lactiferous sinuses
  3. Subareola DCIS not easily identifiable on mammogram
A
  1. Subareola DCIS not easily identifiable on mammogram50% not detectable
60
Q
  1. Colloid tumour of the breast is usually a rounded well defined lesion. Most likely because
  2. Swimming in a pool of mucus
  3. Cells in indian file
  4. Signet ring cells
  5. Intense lymphocytic infiltrate and no desmoplastic response
  6. If granulomas are present this implies can’t be infection or malignancy
A
  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.
  2. Colloid tumour of the breast is usually a rounded well defined lesion. Most likely because:
  3. 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.
  4. Cells in indian file - F - this is evident in invasive lobular carcinoma
  5. Signet ring cells – F - variant of infiltrating lobular Ca .Also seen in pleomorphic LCIS.
  6. Intense lymphocytic infiltrate and no desmoplastic response - F - medullary carcinoma
  7. If granulomas are present this implies can’t be infection or malignancy - F
61
Q
  1. An area of microcalcification was biopsied and revealed LCIS. Which is most likely regarding the calcification
  2. Due to necrotic debris
  3. Due to mucin
  4. Incidental – LCIS doesn’t calcify
A
  1. 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 ??
62
Q
  1. Percentage of breast Ca not associated with a family Hx. Which is most correct
  2. 90 - 95%
  3. 50 - 70%
  4. 20-25%
  5. excluding those with the BRCA gene, 95% cases are nonfamilial
A

**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

  1. 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%
63
Q
  1. Phyllodes
  2. 30-50% will have LN mets at diagnosis
  3. same age as fibroadenoma
  4. low grade lesions difficult to distinguish histologically from fibroadenoma
A
  1. 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”

64
Q
  1. Fibroadenomas . which is false
  2. Increase in size with lactation and infarction,
  3. Usually less than 35
  4. In patients on cyclosporine
  5. Can develop into carcinomas rarely, usually complex fibroadenoma
  6. Neoplasm with precursor dividing into stromal and glandular tissu
A
  1. 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).
  2. Fibroadenomas:
  3. Increase in size with lactation and infarction - T - can cause increased size. Infarction may ultimately result in involution.
  4. Usually less than 35 yrs - T - can occur at any age, but mean age 30yo, median age 25yo. Most common breast tumor under 25yo.
  5. In patients on cyclosporin - T - almost half of women receiving cyclosporin A after renal Tx develop fibroadenomas.
  6. 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.
  7. 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).
65
Q
  1. 20 week fetus, multiple cysts, variable size and decreased liquor seen, maternal grandparent has some sort of polycystic kidney disease:
  2. ARPKD
  3. ADPKD
  4. MCDK
A
  1. 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.
  2. 20 week fetus, multiple cysts, variable size and decreased liquor seen, maternal grandparent has some sort of polycystic kidney disease: (GC)
  3. 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&raquo_space;> 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.
  4. 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).
  5. 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)
66
Q
  1. Ovarian endometroid carcinoma, surprise diagnosis, see what on TVUS:

a. 10% have cervical stenosis
b. 15-30% have endometrial carcinoma or hyperplasia
c. Bilateral involvement in 60%
d. Multilocular cystic mass

A

15-30% have endometrial carcinoma or hyperplasia T - and is the most common malignant neoplasm arising from endometriosis (followed by clear cell Ca).

  1. 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.
67
Q
  1. Distribution of endometriosis, in which order:

a. Ovaries
b. Chest
c. Laparoscopic scar
d. Pouch of Douglas
e. Uterosacral ligaments

A

ovaries > uterine ligts > POD > uterine serosal surface > fallopian tubes > (recto)sigmoid > GU tract > ? laparotomy scars

Ovaries 1 - 80%

  1. 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]
68
Q
  1. Adenomyosis:
  2. Doesn’t exist
  3. Down growth of endometrium
  4. Intramuscular endometrium – same pathology
  5. Benign neoplastic proliferation of endometrial islands
A
  1. 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
69
Q
  1. Live 10 week pregnancy with cystic mass and bilateral ovarian cysts:
  2. Choriocarcinoma in normal pregnancy
  3. Complete mole
  4. Partial mole
  5. Metastatic choriocarcinoma
A
  1. 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

  1. Live 10 week pregnancy with cystic mass and bilateral ovarian cysts: (GC)
  2. 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.
  3. 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.
  4. 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)
  5. Metastatic choriocarcinoma F
70
Q
  1. Presentation of choriocarcinoma, most likely:
  2. Incidental finding on 1st obstetric scan
  3. Hyperemesis
  4. Discharge / bloody
  5. Metastatic disease
A
  1. 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]
  2. 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.
  3. Hyperemesis F - symptoms of complete mole, due to very high BhCG
  4. 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]
  5. 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]
71
Q
  1. 85 yo female and breast cancer risks:
  2. Increased risk with increasing age
  3. Approaches incidence from mets (from other sources)
  4. Risk of DCIS halves, but LCIS stays the same
A
  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. 85 yo female and breast cancer risks: (GC)
  3. 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.
  4. Approaches incidence from mets (from other sources)
  5. Risk of DCIS halves, but LCIS stays the same
72
Q
  1. DCIS removed in 2003:which is false
  2. 10-20% DCIS risk
  3. 1% die of disease
  4. Increased mortality with conservative therapy compared with mastectomy
A
  1. 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.
  2. DCIS removed in 2003: (GC)
  3. 10-20% DCIS risk T - recurrence post lumpectomy: low grade 0-10%, comedocarcinoma 40%
  4. 1% die of disease T - 98% survival after 13 yrs
  5. 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%
73
Q
  1. Tamoxifen – endometrial carcinoma
  2. Associated with BRCA 2
A
  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)

74
Q
  1. Endometrial cancer staging, which is least important:
  2. Involvement of rectal serosa and mucosa
  3. Parametrial involvement, not going to pelvic wall
  4. Involvement of true pelvis
  5. Involvement of myometrium versus external cervix
A

**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]

75
Q
  1. Re: Adenomyosis:
  2. Doesn’t cycle
  3. Looks like a fibroid
A

1 is true

  1. Regarding Adenomyosis, which is true: (GC)
  2. Doesn’t cycle T - glands derive from the stratum basalis of the endometrium, hence don’t undergo cyclical bleeding (unlike endometriosis).
  3. Looks like a fibroid F - most commonly encountered lesion that resembles adenomyosis; differentiation is important as fibroid treated with myomyectomy, whereas adenomyosis requires hysterectomy.  
76
Q
  1. Fetal hydrops associations: which is false
  2. Gastroschisis
  3. Parvovirus
  4. CDH
  5. Trisomy 18
A
  1. Gastroschisis - F - generally not assoc with extra GIT abnormalities (unlike omphalocele).
  2. Fetal hydrops associations: (TW)
  3. Gastroschisis - F - generally not assoc with extra GIT abnormalities (unlike omphalocele).
  4. Parvovirus - T - parvovirus B19 is cytotoxic to fetal blood cell precursors and may cause anemia and hydrops fetalis.
  5. 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).
  6. 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.
77
Q
  1. Trisomy 21:
  2. Cardiac defect 30%
  3. Oesophageal atresia: 5%
  4. Coarctation 20%
A
  1. Oesophageal atresia: 5%
  2. Cardiac defect 30% FALSE - Approx 40%
  3. Oesophageal atresia: 5% TRUE
  4. Coarctation 20% Don’t think so
78
Q
  1. 8 yo trisomy 21 haemarthrosis, splenomegaly and lymphadenopathy
  2. ITP
  3. HUS
  4. ALL
  5. Haemophilia
  6. Amyloid
A
  1. 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).

79
Q

FIGO ENDOMETRIAL Cancer staging:

A

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

80
Q

FIGO CERVICAL cancer staging:

A

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

CDHB Path (22 decks)

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