4 Female GU/ Breast Flashcards

1
Q
Normal epithelium of:
Fallopian tube
Ovary
Prepubertal ectocervix
Prepubertal endocervix
A

Fallopian tube - ciliated columnar
Ovary - flat/ cuboidal
Prepubertal ectocervix - non-keratinised stratified squamous
Prepubertal endocervix - columnar glandular

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2
Q

Bacterial causes of salpingitis (6)

A
Chalmydia trachoma's
Strep
Staph
N. gonorrhoea 
Mycoplasma
Coliforms
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3
Q

Complications of salpingitis

A
Tubo-ovarian abscess/ adherence
Ectopic pregnancy (involving plicae)
Infertility (damage/obstruction of lumen)
Compromised tube function (endometriosis present)
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4
Q

Most common tubal malignancies (3) and precursor

A

Precursor = STIC serous tubal intraepithelial carcinoma - abnormal epithelium (distal tube), nuclear atypia, contained by BM
- p53 mutation

Papillary serous carcinoma
Endometriod carcinoma
1y BRCA mutations

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5
Q

What is in the ovarian:
Cortex
Medulla?

A

Cortex - Outer surface, contains germ cells/ cysts and stroma

Medulla - vessels/nerves, hills cells

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6
Q

Symptoms of PCOS (5)

A
Obesity
Oligomenorrhea 
Hirsuitism
T2 diabetes/ insulin resistance 
Infertility
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7
Q

Mechanism of PCOS and appearance of ovary (4)

A

Cystic follicles (5-15mm) secrete androgens in presence of high LH, low FSH (normally converts androgens to oestrogen)

Appearance:
Subcortical cysts lines by granulose cells
Then by fibrous, thickened cortex outer later
Absence of corpus lute/albicans as no ovulation

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8
Q

Main genes responsible for sporadic ovarian cancer (4)

A

BRCA 1 (and 2)
KRAS
BRAF
P53

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9
Q

Types of ovarian tumour (and likely precursors ± mutations)

A
Epithelial:
HG serous - BRCA1 + p53, STIC
LG serous - KRAS + BRAF
Mucinous - KRAS
Clear cell - endometriosis
Endometriod - endometriosis, loss of PTEN TSG

Germ cell - teratomas
Sex cord stromal tumours

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10
Q

Names of ovarian tumours:

Benign, intermediate and malignant

A

Benign:
solid = adenoma
liquid = cystadenoma

Intermediate/ borderline: tumour with low malignant potential

Malignant:
solid = adenocarcinoma
liquid = cystadenocarcinoma

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11
Q

What is also known as a “chocolate cyst”?

A

Endometriod benign cyst

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12
Q

What 2 ovarian tumour types are associated with endometriosis?

A

Clear cell carcinoma and endometriosis carcinoma

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13
Q

Main characteristics of:
Serous tumours
Mucosal
Endometrioid

A

Serous (25% malignant)- serial involvement, filled with clear fluid, psammoma bodies

Mucosal (10% malignant)- blobs of mucous, multilocular

Endometriod (most malignant) - also habe endometrial carcinoma/ endometriosis

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14
Q

Define Krukenberg tumour

A

Mucinous ovarian tumour which is actually metastases from a tumour of the GIT (typically stomach, appendix, colon) with can mimic 1y ovarian tumour

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15
Q

Genetic factor associated with poor prognosis in ovarian cancer

A

Her2 gene over expression - in 35%

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16
Q

Risk factors/ reducers in ovarian cancer

A

Risk: nulliparity and family hx

Reduce: prolonged use OCP - less ovulation cycles so less change

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17
Q

Sex cord stromal ovarian tumour cell types and hormone produced

A

Leydig and sertoli - androgen

Granulosa/ thecal - oestrogen

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18
Q

Define Meig’s syndrome

A

Benign ovarian fibroma with pleural effusion and ascites

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19
Q

Define Brenner tumour

A

Benign ovarian tumour
Combined surface epithelial and stroll components
Well circumscribed, yellow, solid, unilateral

Transitional epithelium, nuclear grooves, fibrous stroma

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20
Q

Presentation of ovarian tumours (5)

A

Asymptomatic until advanced
SOL: urinary frequency, bowel problems, pain
Torsion: medical emergency, severe abdominal pain
Hormonal effects (if functional tumour)
Ascites (Meig’s/ malignant mets)

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21
Q

Purpose of cervical screening cytology

A

To detect changes in transitional zone (dyskaryosis) due to HPV or CIN

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22
Q

Appearance of normal cervical cells on smear (superficial, intermediate and endocervical)

A

> superficial squamous cells - pink, small central nuclei
intermediate squamous cells - blue, slightly larger central nucleus
endocervical - clumps of columnar cells with basal nuclei

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23
Q

What strains of HPV are most likely to cause cancer in scotland and which are vaccinated against

A

16 and 18

Vaccine = 6, 11, 16, 18

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24
Q

Method of colposcopy

A

1) Visualise cervix with specula and microscope
2) Wash with acetic acid - removes mucus and may stain abnormality white
3) Add iodine - will stain normal different to abnormal
4) Green light filter - view blood vessels
5) Biopsy/ treat if required

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25
Q

How do certain genes in the HPV contribute to cancer?

A

Early genes (E1-7) - take over cell proliferative machinery to replicate virus

Late genes (L1-2) encode proteins for viral capsid

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26
Q

Describe koilocytes

A

Characteristic of HPV, low grade dyskaryosis at minimum

Perinuclear clearing, with dense cytoplasmic condensation around periphery

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27
Q

Epithelium thickness, and nuclear:cytoplasmic ratio in CIN1/2/3

A

Epithelium:
CIN 1 - 1/3
CIN 2 - 2/3
CIN 3 - full thickness

Ratio:
CIN 1 - up to 1/2
CIN 2 - 1/2 to 2/3
CIN 3 - over 2/3

28
Q

Malignant/ premalignant forms of endocervical glandular columnar epithelium

A
premalignant = cGIN (cervical glandular intraepithelial neoplasia)
malignant = adenocarcinoma
29
Q

Treatment options of CIN2/3 and complications

A

> Large loop excision/ bipolar coagulation - scoop out tissue

> Thermoablation/ cold coagulation - burn away affected tissue

Complications:
>Immediate: haemorrhage, pain
>Delayed: 2y haemorrhage, infection, stenosis

30
Q

cervical cancer symptoms

A
Pain
Post coital bleeding
Irregular bleeding
Intermenstrual bleeding
None
31
Q

Infections of the vagina and their characteristic features on histology (5)

A

> Thrush/ yeast - strands (pseudomicelia) and buds
Bacterial vaginosis - coccobaccili on top of squamous cell, looks granular
Trichomonas vaginalis - stuck onto squamous cells and may see flagellae
Actinomyses - looks like a spider, assoc with IUD
Herpes SV - big blue clumps, intranuclear inclusions

32
Q

Describe atrophic vaginitis

A

Post menopausal vaginal inflammation, due to thinning of vagina due to lack of oestrogen

Discomfort, painful intercourse and bleeding

33
Q

Endometriosis theories (2)

A

Metastatic - surgery or retrograde menstruation introduces endometrial tissue elsewhere and it attaches and grows as normal

Metaplastic - endometrial tissue arises from polemic epithelium as it does in embryological development

34
Q

Endometriosis histology:
Normal gland:stoma ratio
Cause of bleeding/ fibrosis etc.

A

GS ratio is still low

Bleeding from endometriosis, causes fibrosis/structures, which causes pain

35
Q

Histological appearance of an endometrial polyp

A

Looks like post-menopausal stroma - no activity
Has thick walled blood vessels
Little cytoplasm
Stroma pink (fibrotic) due to bleeding
Occasionally see cytological atypic/ adenocarcinoma

36
Q

Endometrial hyperplasia/ adenocarcinoma:
Symptoms (1)
Causes (3)
Histology (2)

A

Symptoms: post menopausal bleeding

Causes: increased exposure to oestrogen (anovulatory cycles, obesity, PCOS, oestrogen secreting ovarian tumour, HRT)

Histology: Hyperplasia, increase G:S ratio (less space between glands), ± cytological atypia (bigger rounder nuclei)

37
Q

Endometrial hyperplasia/ adenocarcinoma management

A

Hyperplasia: progesterone therapy (mirena IUD), hysterectomy

Adenocarcinoma: hysterectomy, then treatment based on grade/stage

38
Q

Leiomyoma:
Symptoms
Appearance
Management

A

Symptoms: SOL (urinary infrequency), abnormal bleeding, impaired fertility

Appearance: big round, white/grey, clear edges, whorled out surface, variable size, microscopically identical to normal smooth muscle

Management:
>hormone manipulation (progesterone IUD, GnRH agonist, hormonal therapy),
>stop bleeding (transexamic acid),
>surgery (hysterectomy, myomectomy, uterine artery embolisation)

39
Q

Characteristic appearance of endometrial stroma sarcoma (ESS)

A

“worm like” invasion

Low grade: looks like normal proliferating endometrial stroma with mitosis

40
Q

Describe appearance of normal placental tissue histologically

A

Chorionic villi:
>Odematous stroma
>2 layers of trophoblast (cytoplasms, syncytio)
>Few small blood vessels with metal RBC nuclei in them

41
Q

Describe the components of gestational trophoblastic disease (3)

A

Partial hydatidiform mole: one egg, 2 sperm (triploid)

Complete hydatidiform mole: 0 egg DNA, 2 lots of sperm DNA (either 2 sperm or 1 sperm duplicating DNA)

Choriocarcinoma: rapidly invasive and widely metastasising malignant tumour, but very treatable with chemo

42
Q

Describe appearance of complete and partial mole on histology

A

Partial:
>oedematous villi
>slight trophoblastic proliferation

Complete:
> very oedematous massive villi with central cisterns
> lots of circumferential trophoblastic proliferation
> cells huge and pleomorphic (irregular)

43
Q

FNA and Core biopsy tumour classification

A

FNA = C
Core biopsy = B

1 - normal/ insufficient
2 - benign
3 - probably benign
4 - probably malignant
5 - malignant (b = invasive)
44
Q

Describe phyllodes tumour

A
Fibroadenomatoid lesion - like fibroma has stomal and epithelial parts
>stromal overgrowth and necrosis
>high cellularity and pleomorphism
>irregular margin
>mitotic activity
45
Q

Features of fibrocystic change

And increased risk of carcinoma with hyperplasia

A

Lumps - bigger and more tender in 2nd half cycle
Fibrosis, cysts, apocrine change, epithelial hyperplasia, columnar cell change, calcification

Florid hyperplasia = 1.5x
Atypical hyperplasia = 4x
Insitu carcinoma = 10x

46
Q

Describe appearance of radial scar on mammogram

and what would be done to check for malignancy

A

Stellate appearance

Check presence of myoepithelial tissue

47
Q

Presentation of duct ectasia vs papillary lesion

A

DE:
Nipple discharge (brown/ green)
New nipple inversion
Pain

May have SMOLD
Smokers

PL:
Nipple discharge (bloodied epithelial cells)
Central mass below nipple (not always)
Microcalcification

48
Q

Describe PASH

A

Pseudo Angiomatous Stomal Hyperplasia (benign)

Rapidly growing hard palpable lump
With lots of small vessels and myofibroblasts
Inflammatory skin changes

49
Q
Age of onset of:
PASH
Granulomatous mastitis
Fibrocytsic change
Fibroadenoma
Diabetic mastopathy
Breast carcinoma
A
Fibroadenoma - 20-30
Fibrocytsic change - 30-40
Diabetic mastopathy - <30
Granulomatous mastitis - mid 30s (33)
PASH - premenopausal
Breast carcinoma - 40-70
50
Q

Difference between DCIS and LCIS

A

DCIS - can be removed and cured
>Abnormal cell proliferation
>Enlarged glands
>Necrosis/ calcification

LCIS can occur anywhere in either breast, need regular monitoring
>No calcification/ lump
>Lobules and ducts expanded - abnormal proliferation

51
Q

3 factors considered when grading breast carcinoma

Grading system used for invasive ductal carcinoma

A

Tubules
Mitotic activity
Pleomorphism

52
Q

Characteristic feature of lobular carcinoma on histology

A

Signet ring cells

Aligned one behind the other

53
Q

Scoring system for hormone receptor in breast cancer and treatment outcome

A

Allred scoring system:
0-2 receptors - negative, no treatment
3-5 - positive, poor treatment response
5-8 - positive, good treatment response

54
Q

Treatment options for breast cancer (hormone receptor +ve) (2)

A

Tamoxifen - ER antagonist

Aromatase inhibitors

55
Q

Describe nottingham prognostic index and purpose

A

Grade: 1 point per grade (1-3)
Size: point = size in cm x0.2
Nodal status: 0=1, 1-3=2, 4+=3

Treatment, followup and prognosis

56
Q

Treatment for HER2 positive cancers, and testing method for HER2

A

Herceptin/ transtuzumab

57
Q

Other sources breast cancers other than carcinoma

A

Mets
Lymphoma
Sarcoma (Phyllodes or denovo)
Angiosarcoma - previous radiotherapy

58
Q
Describe the terms used in cancer subtypes:
Luminal
Basal
HER2
Normal
A

Luminal - ER/PR + (a/b = low/high proliferative)
Basal - ER/PR/HER2 -
HER2 - HER2 +, ER/PR -
Normal - benign

59
Q

Toxic side effects of cancer chemotherapy general (7)

A

> Hair loss
Damage GI epithelium - X solids > weaker
Bone marrow suppression - anaemia, bleeding, infection
Liver, heart, kidney
Growth depression children
Infertility/ sterility
Teratogenicity

60
Q

Alkylating agents cancer chemo:

MOA and main names (3)

A

MOA: cross link DNA strands to prevent separation for replication, and also inhibit transcription (by-product)

Melphalan
Cyclophosphamide
Cisplatin

61
Q

Antimetabolites cancer chemo:

MOA and main names (4)

A

Methotrexate: folate antagonist (prevents dihydrofolate) > X nucleotide synthesis> X DNA/RNA

5-hydro uracil: pyramidine analogue (thymine) > X thymidine > X DNA

Mercaptopurine: purine analogue > flash nucleotides made> into DNA> helix disrupted

Cytarabine: inserts into DNA > inhibits DNApol > chain termination

62
Q

Cytotoxic antibiotics cancer chemo:

MOA and main names (2)

A

Dactomycin: binds at minor groove (cis molecules) > inhibits RNA pol

Doxorubicin: binds DNA backbone between strands > local uncoiling> X transcription

63
Q

Microtubule inhibitor cancer chemo:

MOA and main names (1)

A

Vincristine (vinka alkyloid)

Blocks cell division at anaphase/metaphase
>Binds microtubule protein > blocks tubular polymerisation & spindle formation

64
Q

Steroid hormones/antagonists cancer chemo:

MOA and main names (4)

A

Prednisone: > prednisolone - suppress lymphocyte growth

Tamoxifen: ER receptor blocker (ER+ BrCa)

Bicalutamide: testosterone receptor antagonist (Test dept PrCa)

Prostap: LHRH agonist > dec LH secretion> dec testosterone (Test dept PrCa)

65
Q

Premalignant variants of skin cancer:
Squamous cell carcinoma
Melanoma

A

SCC - Bowen’s disease/ actinic keratosis

Melanoma - melanomi in-situ/ lentigo maligna