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Phase 3 > Female GU & Breast > Flashcards

Female GU & Breast Flashcards

1
Q

Describe the normal anatomy of the breast

A

The breast consists of

  • 15-20 lobules separated by ligaments of Cooper
  • Lobes contain alveoli, which contain lactocytes
  • Alveoli are surrounded by myoepithelial cells (contractile)
  • Lobes are connected by a ductal system
  • Oxytocin stimulates the contraction of myoepithelial cells, pushing milk into lactiferous ducts & towards the nipple
  • Ducts converge at the lactiferous sinus, below the nipple
  • Glandular tissue (lobules) and lactiferous ducts are lined by a characteristic epithelium with 2 layers: inner (luminal) & outer (myoepithelial)
  • Nipple has an average of 9 openings, surrounded by the areola
  • Montgomery tubercles (glands) secrete a sebaceous fluid that lubricates the nipple
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2
Q

Describe the blood supply of the breast

A
  • Internal thoracic artery (medially)
    > Anterior perforating branches
  • Axillary artery (laterally)
    > lateral thoracic artery
    > pectoral branch of acromioclavicular artery
    > subscapular artery
  • Intercostal arteries (lateral perforating branches)
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3
Q

Describe the lymphatic drainage of the breast

A
  • Axillar nodes
    > Apical group
    > Central group
    > Anterior group
    > Lateral group
  • Internal thoracic nodes
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4
Q

Describe the investigations used in breast pathology

A
  • Clinical examination: both breasts, axilla, supraclavicular nodes
  • Imaging: ultrasound, 2 view mammography, MRI
  • Biopsy
    > Fine needle aspiration (FNA): cytology
    > Core biopsy or vacuum assisted biopsy: histology
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5
Q

List and describe developmental abnormalities of the breast

A
  • Ectopic (heterotopic) breast tissue
    > Often on the milk line between axilla and groin
    > Nipple-areolar and glandular tissue may be present +/- nipple
    > Any breast disease may occur in heterotopic breast tissue
  • Breast hypoplasia
    > Associated with ulnar-mammary syndrome, Poland’s syndrome, Turner’s syndrome & congenitla adrenal hyperplasia
  • Macromastia
    > Stromal overgrowth leading to excessive breast size
    > Can begin at puberty (juvenile hypertrophy) or pregnancy (gestational hypertrophy)
  • Breast asymmetry
    > Mild is common, severe developmental may be distressing (corrective surgery)
  • Nipple inversion
    > Common and usually normal unless it is a new inversion
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6
Q

Describe 1) acute mastitis 2) periductal mastitis/duct ectasia

A
  1. Acute mastitis (puerperal or lactational)
    > Cellulitis associated with breastfeeding
    > Skin fissuring may let bacteria in - milk stasis favours their growth leading to infection of breast tissue
    > Abscesses may require incision & drainage as well as antibiotics
  2. Periductal mastitis/duct ectasia
    > Dilation of central lactiferous ducts
    > Periductal chronic inflammation
    > Scarring
    > Calcified luminal secretions may be seen on mammogram
    > Symptoms may include discomfort, mass, nipple retraction/inversion, green-brown nipple discharge
    > Associated with smoking and aging
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7
Q

Describe the conditions which may lead to granulomatous inflammation of the breast tissue

A
  • Systemic disease including sarcoidosis and infections such as tuberculosis, leprosy
  • Idiopathic granulomatous mastitis
    > Lobule-centred non-necrotising granulomatous inflammatory process
    > Tendency to recur after excision but may respond to steroids
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8
Q

Describe the following inflammatory conditions of the breast
> Foreign body reactions
> Recurrent subareolar abscesses
> Fat necrosis

A

> Foreign body reactions can occur around breast implants & may lead to scarring, fibrosis, capsular contractures
> Lead to discomfort and distortion of the breast
> Includes reactions to silicone leakage after implant rupture

> Recurrent subareolar abscesses
> May be associated with mamillary fistula, squamous metaplasia of lactiferous ducts and smoking

> Fat necrosis
> May follow trauma, is benign but biopsy may be required to rule out cancer

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9
Q

List the conditions which fall into the class of inflammatory pathology of the breast

A
  • Acute mastitis
  • Periductal mastitis/duct ectasia
  • Granulomatous inflammation of the breast
  • Inflammatory breast cancer
  • Foreign body reactions
  • Recurrent subareolar abscesses
  • Fat necrosis
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10
Q

List the conditions which may fall under the class of benign conditions of the breast

A
  • Fibrocystic changes
  • Fibroadenoma
  • Phyllodes tumour (also malignant)
  • Pure adenomas
  • Nipple adenoma
  • Hamartoma of the breast
  • Benign granular cell tumours
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11
Q

List the conditions which may fall under the class of malignant conditions of the breast

A
  • Ductal carcinoma in situ
  • Invasive ductal carcinoma
  • Lobular carcinoma in situ
  • Invasive lobular carcinoma
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12
Q

Describe the spectrum of fibrocystic change in the breast

A
  • Cysts: small & large
    > A galactocoele is a rare milk-filled cyst in the breast
  • Adenosis: increased amounts of glandular tissue
    > Sclerosing adenosis refers to a benign proliferation of distorted glandular tissue & stroma
  • Stromal proliferations
    > Diabetic fibrous mastopathy
    » Stromal fibrosis with infiltrating lymphocytes associated with type I diabetes
    > Pseudo-angiomatous stromal hyperplasia (PASH)
    » Proliferation of myofibroblasts causes a mass & may require biopsy to exclude malignancy

> Epithelial hyperplasia +/- atypia (increased cancer risk)
> Includes ductal and lobular hyperplasia
> Both have features in common with low grade ductal or lobular carcinoma in situ, different in terms of cell proliferation
> Associated with microcalcifications

> Apocrine metaplasia of cyst epithelium
> Characterised by large, rounded epithelial cells with copious granular eosinophilic cytoplasm & apical projections

> Columnar cell lesions
> Columnar cell change and columnar cell hyperplasia +/- atypia; associated with microcalcifications

> Intraductal papilloma
> benign tumour of the epithelial lining of the mammary ducts; harmless if no atypia
> Can present with bleeding from nipple
Multiple papillomas (papillomatosis) are more likely to be associated with breast malignancy

> Radial scars
> benign lesions characterised by a fibrotic core with elastic fibres, trapped glands & pseudo-infiltrative appearance
> Complex sclerosing lesions if >10mm
> Atypical proliferations may be present and increase cancer risk

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13
Q

Describe the different types of benign neoplasms which may be found in the breast

A
  • Fibroadenoma
    > Characteristic overgrowth of epithelium and stroma, resembling a giant lobule
    > Patterns; pericanalicular, intracanalicular
    > Hormone sensitive & regress after menopause
    > Firm, non-tender, mobile, <25-30mm
    > Stroma is similar to the stroma of normal terminal ductal lobular unit (TDLU)
    > Giant fibroadenoma - 100+mm, juvenile fibroadenoma in girls <18
  • Phyllodes tumour aka cytosarcoma phyllodes
    > Combines epithelium and mesenchyme but with more cellular stroma, mitotic activity cytological atypia & infiltrative border compared to fibroadenoma
    > Behaviour can vary (malignant or benign)
  • Pure adenomas: tubular or lactating
    > Lack prominent stromal element of fibroadenomas
  • Nipple adenoma aka papillomatosis of nipple ducts/erosive adenomatosis (uncommon):
    > Benign but can mimic Paget’s disease of the nipple (malignant)
  • Hamartoma of the breast (uncommon
    > Benign - forms a discrete, smooth, painless mass of glandular, fatty & fibrous connective tissue
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14
Q

Describe Paget’s disease of the nipple

A

Rare type of cancer of the nipple-areolar complex often associated with underlying carcinoma

Mimics eczema - persistent soreness, itching, erythema & scaling

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15
Q

List the risk factors for breast cancer (& protective factors)

A
  • Early menarche
  • Late menopause
  • Being older at first pregnancy/childbirth
  • Oral contraceptive use
  • Hormone replacement therapy (HRT)
  • Obesity
  • Tallness
  • Denser breast tissue on mammography
  • Alcohol
  • Positive family history
  • Breast cancer genetic syndromes: BRCA1/2, P53 - Li Fraumeni Syndrome

Protective: early pregnancy and childbirth, exercise and breastfeeding

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16
Q

Describe the symptoms of breast cancer

A
  • New lump or thickening in the breast of axilla
  • Altered shape, size or feel of the breast
  • Pain
  • Skin changes
    > Puckering or dimpling
    > Peau d’orange (skin oedema)
    > Rash or redness
  • Nipple changes
    > Tethering/inversion
    > Discharge
    > Eczema-like changes (Paget’s disease)
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17
Q

Describe the investigations used in breast cancer

A
  • Clinical examination: inspection in different positions, palpation
  • Imaging: ultrasound, X-ray mammography, MRI
  • Fine needle aspiration cytology with microscopy of cells recovered
  • Core biopsy (guided by imaging) with microscopy of tissue sections
  • Excisional biopsy - diagnostic or therapeutic
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18
Q

Describe breast screening

A

Women between 47-73 are invited for 2-view mammographic breast screening every 3 years

  • Microcalcification is often present in invasive carcinoma and may be detectable on X-ray mammography
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19
Q

Describe the surgical treatments for breast cancer

A
  • Surgery aims to remove all cancer tissue with margins free of cancer
  • Wide local excision (WLE) or lumpectomy + radiotherapy - achieves comparable local control + overall survival to mastectomy
  • Larger cancers may still require mastectomy to achieve clear margins
    > Axillary clearance is not necessary if sentinel node biopsy is negative; axillary clearance has significant morbidity e.g. lymphoedema, restriction of arm movement
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20
Q

Describe non-surgical treatments for breast cancer

A
  • Steroid hormone receptors: 80% of breast cancers overexpress oestrogen & progesterone receptor
    > ER/PR positive carcinomas respond to endocrine treatment
    > E.g. Tamoxifen: in breast, an ER antagonist but in bone & endometrium, it is an agonist, elevating endometrial cancer risk
  • Aromatase inhibitors e.g. letrazole, anostrazole
    > Block conversion of adrenal androgens to oestrogens as it does in adipose tissue; prevents oestrogen stimulation of tumour growth
  • Her2 positive cancers: overexpression of Her2 has a worse prognosis
    > Can be treated with monoclonal antibody trastuzumab (Herceptin)
  • Chemotherapy
    > Important to prevent metastatic relapse, especially in ER-PR-HER2- cancers as these do not respond to endocrine treatment
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21
Q

Describe the grading and staging of breast cancer

A
  • Stage: carcinoma size, lymph node involvement & metastasis
  • Grade: based on 3 histological properties
    > Nuclear pleomorphism
    > Number of mitoses per mm2
    > Degree of gland formation by cancer cells

Grade 1: well-differentiated & slow growing
Grade 3: poorly differentiated & fast growing

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22
Q

Describe the Nottingham Prognostic Index (NPI)

A

Combines grade, tumour size in cm and stage into a numerical prognostic index

Graed + stage + size (cm) / 5

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23
Q

Describe the divisions of breast cancer

A
  • Invasive ductal carcinoma (IDC)
  • Invasive lobular carcinoma (ILC)
  • Special types
    > 70% ductal
    > 10-15% classical lobular & variants - alveolar, solid, pleomorphic, tubular-lobular
    > Papillary/micropapillary
    > Medullary
    > Tubular, cribriform
    > Mucinous
    > Acinic cell, adenoid cyst, apocrine, glycogen-rich, lipid-rich, oncocytic, secretory, sebaceous
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24
Q

Describe precursor lesions for breast cancer

A
  • Ductal epithelial hyperplasia +/- atypia (low grade dysplasia)
  • Lobular epithelial hyperplasia +/- atypia (low grade dysplasia)
  • Carcinoma in situ (high grade dysplasia)
    > aka ductal carcinoma in situ (DCIS) and lobular carcinoma in situ (LCIS)
    > Proliferation of markedly abnormal epithelial cells within the basement membrane
    > No extension into breast stroma
    > No communication with blood vessels or lymphatics so no possible metastases
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25
Q

Describe the histology of the Fallopian tube

A
  • Tubal structure with a muscular wall covered by peritoneum
  • Has a fimbrial end with finger-like projections
  • The internal aspect has a complex arrangement of plical folds
  • These are covered by serous epithelium, which contains cuboidal cells with round/ovoid nuclei, cilia and secretory cells
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26
Q

Describe the histology of the ovary

A
  • Appearance varies depending on patient’s age, menopausal status and in pregnancy
  • Peripheral cortex contains numerous follicles containing ova (germ cells)
    > Corpora lutea and corpora albicantes are seen here during menstruation (corpora albicantes remain post-menopausally)
  • Central medulla
    > Stroma: spindle-shaped cells and collagen fibres
    > Blood vessels
    > Leydig cells
  • Mesothelial cells form the peritoneal covering
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27
Q

Describe the embryological development of the ovary and Fallopian tube

A
  • Germ cells (endodermal) originate from the yolk sac and by week 5-6 of gestation migrate to the urogenital ridge
  • Mesodermal epithelium of this ridge then forms the epithelium & stroma of the ovary
  • Around week 6, invagination and fusion of the coelomic epithelium and stroma form the 2 Mullerian ducts
    > Ducts grow downwards towards the pelvis
    > Fuse together and then with the urogenital sinus
    > Unfused portions become the Fallopian tube
    > Fused portion becomes the uterus & vagina
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28
Q

Describe non-neoplastic ovarian cysts

A
  • Follicular cysts: normally part of the menstrual cycle so contain a central oocyte
  • Luteal cysts: large corpus luteum which remains after ovulation
  • Inclusion cysts: infoldings of the surface peritoneum which become trapped within the ovarian stroma
    > result in small cysts lined by mesothelial cells within ovarian cortex
  • Polycystic ovary syndrome (PCOS): ovaries contain a large number of follicular cysts, many of which lack a central oocyte
    > Patients may be anovulatory or have irregular periods
    > Androgen excess can result in hirsutism, acne and weight gain as well as fertility issues
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29
Q

Describe ovarian stromal hyperplasia

A
  • Uniform enlargement of the ovary usually affecting post-menopausal women
  • Stromal hyperplasia but no luteinised cells
    > if luteinised cells are present, this is termed stromal hyperthecosis - greater incidence of hyperandrogenism
  • Histologically appears as
    > Ill-defined white/yellow nodules macroscopically
    > Microscopy shows replacement of the cortex and medulla by nodules of ovarian stroma
30
Q

Describe pelvic inflammatory disease (PID) and tubo-ovarian abscess

A
  • Part of the spectrum of pelvic inflammatory disease
  • Underlying cause is usually sexually transmitted: Chlamydia trachomatis, Neisseria gonorrhoea
  • Enters the gynecological tract via the vagina and initially causes cervical inflammation
    > Ascending infection results in salpingitis
  • PID presents with abdominal/pelvic pain, adnexal tenderness, fever and vaginal discharge
  • PID is treated with antibiotics and occasionally surgical resection of abscesses
  • Complications of PID include tubo-ovarian abscess formation and fibrosis or fusion of tubal plicae resulting in increased risk of infertility and ectopic pregnancy
31
Q

Describe the histological appearance of acute salpingitis

A
  • Aggregates of macrophages and neutrophils
  • Apoptotic debris
  • Pus filling the lumen of the fallopian tube
32
Q

Describe endometriosis, including sites, clinical symptoms and causes

A
  • Endometrial constituents (glands and stroma) occur outwith the endometrial cavity

> Myometrium, uterine surface, ovaries, large and small bowel, appendix, mucosa of cervix, vagina and fallopian tube, laparotomy scars, pleural cavity, peritoneal surfaces (uterine ligaments, rectovaginal septum)

  • Ovarian endometriosis can result in the formation of blood-filled cysts (endometriomas aka chocolate cysts)
  • Abnormally located endometrium continues to bleed and can result in scarring and adhesion formation in adjacent tissues (rarely tumours can develop)
  • Clinical symptoms: dysmenorrhoea, pelvic pain, infertility
  • Causes
    > Metastatic theory: retrograde menstruation/surgical procedures introduce endometrium to sites outwith uterine cavity
    > Metaplastic theory: endometrium arises directly from the coelomic epithelium (i.e. peritoneum) of the pelvis (supported by endometriosis reaching pleural cavity sometimes)
33
Q

List the types of ovarian tumours

A
  • Serous cystadenoma
  • Serous carcinoma
  • Mucinous cystadenoma
  • Clear cell carcinoma
  • Endometrioid carcinoma
  • Mature teratoma
  • Other germ cell tumours
  • Fibroma
  • Adult granulosa cell tumour
  • Elsewhere in the body metastasising to the ovaries
34
Q

Describe ovarian serous cystadenomas

A
  • Can be benign, borderline or malignant, derived from surface epithelium

Benign serous cystadenoma:
- Cyst has a thin wall which is lined by epithelium
identical to tubal/serous epithelium in the fallopian tube
> One cell thick with no tufts, papillary areas or solid growth; no cytological atypia
> Treatment: removal of cyst; no risk of malignancy

Borderline serous cystadenoma:
- Borderline tumours have more complex growth patterns compared to benign tumours; some cytological atypia
- Behaviour is difficult to predict; can recur or develop into low grade serous carcinoma
- Frank evidence of invasion is absent - no growth into underlying structures of ovary
- Histology - papillary & micropapillary structures grow
> Branches of stroma covered with epithelium
> Aggregates of epithelial cells with no stromal core
> Calcified areas can appear - psammoma bodies

35
Q

Describe ovarian serous carcinoma

A

Low grade serous carcinoma
- Slowly progressive surface epithelium tumour with recurrences following excision
> Do not respond well to chemotherapy
> Molecular abnormalities: BRAF/KRAS mutations
- Histology shows areas of frank invasion

High grade serous carcinoma
- Commonest type of ovarian carcinoma
- Usually present in peri-menopausal or post-menopausal women
- Originates in the Fallopian tube but present in the ovary & elsewhere after metastasis

  • Causes:
    > Precursor lesions in the fallopian tube (serous tubal intraepithelial carcinoma)
    > Can be seen in younger patients with BRCA or P53 mutations
  • Treatment: surgery + chemotherapy
  • Histology: abnormal differentiation (no resemblance to original tissue), mitotic figures and areas of necrosis
36
Q

Describe ovarian mucinous cystadenomas

A
  • Can be benign, borderline or malignant
  • Borderline mucinous cystadenoma
    > Mucin vacuoles within luminal aspect of the cell
    > No frank invasion of stroma making up the wall of the cyst

> Frank invasion - malignant mucinous tumour (carcinoma); can be difficult to differentiate from metastases from GI tract

37
Q

Describe ovarian clear cell carcinoma

A
  • Associated with endometriosis; usually large and solid or cystic
  • Treatment: surgery; resistant to platinum-based chemotherapy
  • Histology
    > High trade tumours with different growth patterns - tubular, cystic, papillary, solid (don’t always have clear cytoplasm)

> Can be difficult to differentiate from high grade serous carcinoma but do NOT have mutations in p53

> Hobnailing: large nuclei, little cytoplasm means nuclei stick to lumen of glands

> Formation of hyalin globules (pink structures within lumen of glandular structures or inside cells)

38
Q

Describe mature teratomas

A
  • Usually found in women of reproductive age
  • Consist of mature tissues derived from one or more embryonic germ layers (ectoderm, mesoderm, endoderm)
  • Most are cystic but have solid areas depending on the tissues which have developed
    > Contain hair and greasy sebaceous material, sometimes cartilage, bones & teeth
    > Microscopically different tissues are identified: skin, respiratory epithelium GI, thyroid, adipose, glial tissue…
  • Require thorough sampling
    > Immature teratomas: embryonal/foetal tissue can be malignant and recur/metastasise
    > Somatic malignancies: small number of cases
39
Q

Describe an ovarian fibroma

A
  • Benign: vary in size and are firm & white with a lobulated surface, can be bilateral
    > Often present with non-specific symptoms e.g abdominal pain if mass is large or are incidental findings

> Meig’s syndrome: some patients have an ovarian fibroma associated with ascites

> Microscopy
- Small bland spindle-shaped cells & collagen
- No cytological atypia, few mitotic figures, no necrosis

40
Q

Describe adult granulosa cell tumours

A

Low grade malignancy, usually unilateral & confined to ovary
> Variable size, solid/cystic appearance

Most do not recur or metastasise

  • Oestrogen-secreting tumour
    > results in abnormal vaginal bleeding e.g. menorrhoea, amenorrhoea, post-menopausal bleeding
  • Occasionally, androgen-secreting tumour
41
Q

Describe symptoms of ovarian cancer

A
  • Abdominal distension
  • Urinary symptoms
  • GI symptoms (due to compression by ovarian mass)
  • Torsion (larger neoplasms), obstruction of venous return causing severe pain and peritonitis
42
Q

Describe developmental abnormalities of the uterus

A

Developmental abnormalities of the uterus are related to abnormalities in the fusion of the Mullerian ducts

  • Class U1: dysmorphic uterus
    > T-shaped, infantilis, others
  • Class U2: septate uterus
    > Partial or complete
  • Class U3: bicorporeal uterus
    > Partial, complete, bicorporeal septate
  • Class U4: hemi uterus
    > With or without rudimentary cavity
  • Class U5: aplastic uterus
    > With or without rudimentary cavity
43
Q

Describe the histology of the endometrium during the different phases of the menstrual cycle

A
  • Proliferative phase
    > Oestrogen drives thickening of the endometrium
    > Dividing cells can be seen (mitotic figures)
    > Gland:stroma ratio is low - each gland is separated by stroma
    > Tubular glands
    > Cells within glands: cuboidal cells, elongated, ovoid nucleus, stratification (different heights of cells)
    > Cells within stroma: small with round/ovoid nuclei
  • Secretory phase
    > Following ovulation, corpus luteum starts to produce progesterone
    > Coiled glands
    > Gland:stroma ratio is still low
    > Small gap between nucleus and basement membrane - subnuclear vacuoles found here
    > As secretory phase progresses, glands become more complex, vacuoles disappear and secretions appear in lumen of gland
  • Menstrual phase
    > Fragmentation of endometrium
    > Condensation of stroma - epithelium has surrounded stromal cells
    > Inflammatory cells (neutrophils) can be seen
    > Areas of necrosis and blood
44
Q

Describe the histology of the endometrium in post-menopausal women

A
  • Cystic atrophy
  • Thin endometrial lining as it is not simulated by hormones
  • Nuclei are small, no mitotic figures, no evidence of secretion - atrophic endometrium
45
Q

Describe the histology of the myometrium

A
  • Smooth muscle bundles comprising much of the uterus; long nucleus
  • No mitotic activity as the muscle does not change during the menstrual cycle
46
Q

Define adenomyosis

A

Presence of endometrial tissue within myometrium

47
Q

Describe endometrial polyps and their microscopy

A
  • Exophytic masses of variable size which project into endometrial cavity
  • Associated with tamoxifen in some cases
  • Microscopy
    > Haphazardly arranged glands with preservation of a low gland:stroma ratio
    > Thick walled blood vessels & fibrous stroma
    > Glands are usually inactive but can show proliferation, secretory changes or metaplasias
    > Can resemble post-menopausal atrophic endometrium
    > occasionally cytological atypia or frank adenocarcinoma can be found in polyps
  • Presentation: abnormal bleeding
  • Treatment: hysteroscopy in outpatient clinic
48
Q

Describe endometrial hyperplasia and adenocarcinoma

A
  • Conditions associated with prolonged oestrogenic stimulation of the endometrium
  • Causes
    > Anovulatory cycles
    > Endogenous sources of oestrogen e.g. obesity, PCOS, oestrogen-secreting ovarian tumours
    > Exogenous sources of oestrogen e.g. oestrogen-only HRT
  • Symptoms
    > Postmenopausal bleeding
    > Menorrhagia, oligomenorrhoea in pre-menopausal women
  • Microscopy:
    > Endometrial hyperplasia - increase in the gland:stroma ratio +/- cytological atypia
    > Atypical endometrial hyperplasia is a known precursor of endometrioid adenocarcinoma (stroma is lost & glands fuse together)
  • Management:
    > Hyperplasia: progesterone therapy (Mirena IUS) or hysterectomy
    > Endometrial adenocarcinoma: hysterectomy
49
Q

Describe leiomyomas including symptoms, appearance and management

A
  • Benign smooth muscle tumour of the myometrium aka fibroid
  • May be single or multiple
  • Macroscopic appearance
    > Sharply demarcated round grey-white tumours with a whorled cut surface
    > Variable in size and resemble normal smooth muscle
  • Symptoms
    > Asymptomatic
    > Abnormal bleeding
    > Urinary frequency if large
    > Impaired fertility
  • Management
    > Medical:
    » Progesterone-secreting IUS
    » Hormonal therapies
    » Tranexamic acid
    » GnRH agonists

> Surgical
> Uterine artery embolisation
> Myomectomy
> Hysterectomy

50
Q

Describe the symptoms and pathology of leiomyosarcoma

A
  • Uncommon malignant smooth muscle tumour of the myometrium

Symptoms: initially asymptomatic, then bleeding or pain

Pathology
> Macroscopy:
» Bulky invasive masses or polypoid
» Necrosis
» Haemorrhage
» Variable cut surface

> Microscopy
> Overt cytological atypia
> Necrosis
> Mitotic activity
> Infiltrative margin

51
Q

Describe endometrial stromal sarcoma (ESS)

A
  • Rare groups of tumours of the endometrial stroma; can be low or high grade
  • Diffusely infiltrative “worm like” growth pattern
  • Microscopy: low grade tumour cells resemble cells of proliferating endometrial stroma with mitoses
    > no glands, unlike adenomyosis
52
Q

Describe gestational pathology

A
  • Gestational trophoblastic disease

> Hydatidiform moles aka molar pregnancy
Present with either spontaneous miscarriage or abnormalities detected on ultrasound

> > Partial mole: fertilisation of one egg by 2 sperm: triploid karyotype
- Microscopy shows no foetus and oedematous villi & subtle trophoblast proliferation
- Risk of invasive mole - invades & destroys the uterus

> > Complete mole: fertilisation of an egg with no genetic material, usually by one sperm which duplicates its chromosomal material OR egg with no genetic material fertilised by 2 sperm (diploid karyotype, usually 46XX)
- Microscopy: markedly enlarged oedematous villi with central cisterns and circumferential trophoblast proliferation
Risk of invasive mole & choriocarcinoma

  • Frankly malignant tumours: choriocarcinoma
    > Rapidly invasive & metastasises widely but treatable with chemotherapy
53
Q

Describe the histology of the endocervix and ectocervix

A

Endocervix: lined by mucin-secreting columnar glandular mucosa

> Physiological squamous metaplasia occurs between endocervix and ectocervix epithelial

Transformation zone: zone where glandular cells and squamous cells meet, usually around neck of cervix leading onto endocervical canal

Ectocervix
> Vagina: non-keratinising stratified squamous epithelium
> Vulva: keratinising stratified squamous epithelium (nuclei may disappear)

54
Q

List infections which may affect the vagina and cervix

A
  • Human Papilloma Virus (HPV)
  • Chlamydia trachomatis
  • Gonorrhoea
  • Herpes simplex virus (HSV)
  • Trichomonas vaginalis
  • Candida albicans or “thrush”
  • Actinomyces
  • Bacterial vaginosis
55
Q

Describe cervical polyps

A
  • Benign growth most of the time
  • overgrowth of connective tissue with epithelial covering; may bleed post-coitally
56
Q

Describe cervical screening

A

Women aged 20-60 are invited to have a cervical smear every 3 years

  • Designed to identify pre-cancerous changes (dyskariosis) in cervical smears so patients can be referred for colposcopy

> Dyskariosis: nuclear enlargement, dense hyperchromasia, coarse chromatin clumping

  • In cervical biopsies, precancerous changes are called cervical intraepithelial neoplasia (CIN)
  • Smear reporting

> Negative: repeat routinely in 3yrs

> Borderline nuclear abnormality: repeat 6 months, x3 BNA refer for colposcopy
e.g. koilocytosis: clearing of cytoplasm around nuclei due to HPV infection

> Dyskariosis, any severity: refer colposcopy
> Low grade is CIN1
> High grade is CIN2 or CIN3: expanded proliferation zone, mitotic further up in epithelium (not just basal layer) due to abnormal cell proliferation & failure of maturation

57
Q

Describe cervical carcinoma including symptoms, risk factors and treatment

A
  • Invasive squamous cell carcinoma when basement membrane is breached
    > Other variants include adenocarcinoma, clear cell carcinoma & adenosquamous carcinoma
  • Symptoms:
    > Post-coital bleeding
    > Intermenstrual bleeding
    > Irregular vaginal bleeding
    > Pain
    > Asymptomatic
  • Risk factors
    > HPV
    > Age at first sexual intercourse & number of sexual partners
    > Smoking
    > Method of contraception: OCP v barrier
    > Immunosuppresion
    > Circumcision in males - protective
  • Treatment
    > Early lesions treated surgically via Large Loop Excision of Transformation Zone (LLETZ) or simple/radical hysterectomy

> Advanced: radiotherapy + chemotherapy

58
Q

What is meant by cGIN?

A

Endocervical glandular epithelium undergoing premalignant change: cervical glandular intraepithelial neoplasia
> Malignant change from glandular epithelium is adenocarcinoma
> HPV associated and less common

59
Q

Which structures does the vulva consist of?

A
  • Mons pubis
  • Labia minora
  • Clitoris
  • Vestibular bulbs
  • Vulvar vestibule
  • Urinary meatus
  • Vaginal opening
  • Hymen
  • Bartholin’s and Skene’s vestibular glands
60
Q

Describe the different conditions which may affect the vulva (non-neoplastic)

A
  • Inflammatory skin conditions that affect hair-bearing skin e.g. psoriasis, eczema, allergic dermatitis
  • Infections
    > Vulval warts
    > Candida
    > Infection in hair follicles (folliculitis)
    > Bartholin’s abscess
  • Cysts
    > Epidermal inclusion cyst
    > Bartholin’s cyst - obstruction of Bartholin’s duct
61
Q

Describe the different neoplastic conditions which may affect the vulva

A

Leukoplakia may represent benign, premalignant or malignant lesions
» may be caused by lichen sclerosus et atrophicus - inflammatory dermatitis associated with neoplastic progression
» Caused by squamous hyperplasia

  • Rarely, may be benign or malignant
    > Neurofibromas, angiomas
    > Skin adnexal tumours
    > Carcinomas, melanomas
    > Sarcomas
  • Mainly invasive squamous cell carcinoma
    > associated with VIN (vulval intraepithelial neoplasia), also CIN & invasive cervical cancer
    > Usually related to high risk HPV 16/18
    > Warty or basaloid cancer
    > Can be associated with dermatoses in older women; mostly well-differentiated & keratinising cancers, not associated with HPV infection
    > Adjacent squamous hyperplasia and/or lichen sclerosus et atrophicus are common
62
Q

Describe the general toxic effects of chemotherapy

A
  • Bone marrow suppression
    > Anaemia
    > Immune depression
    > Infection risk
    > Impaired wound healing
  • Loss of hair
  • Damage to gastrointestinal epithelium
  • Liver, heart, kidney
  • In children - depression of growth
  • Sterility
  • Teratogenicity
63
Q

List the different types of cancer chemotherapy drugs

A
  • Alkylating agents
  • Antimetabolites
  • Cytotoxic antibiotics
  • Steroid hormones & antagonists
64
Q

Describe the different types of alkylating agents and their mode of action

A

Alkylating agents form strong covalent bonds with DNA
> Interfere with transcription and replication
> Most have 2 reactive groups which allow the drugs to cross-link within one DNA strand or across 2 strands of DNA

  • Nitrogen mustards
    > Mechlorethamine: lymphoma (HL & NHL)
    > Melphalan: fusion of mechlorethamine w/ phenylalanine - multiple myeloma, ovarian & breast cancer
    > Cyclophosphamide: prodrug requiring activation in the liver, used to treat many cancers
    > Chlorambucil, cyclophosphamide, ifosfamide
  • Cisplatin: stops DNA replication, targets N7 of purine nucleotides; resistance from nucleotide excision repair mechanisms and efflux transporters for copper
  • Temozolamide
  • Lomusine: active in CNS
  • Busulphan: selective effect on bone marrow
65
Q

Describe the different types of antimetabolites and their mode of action

A
  • Antimetabolites interfere with nucleotide synthesis or DNA synthesis

> Nucleotide synthesis: antifolates

> > Methotrexate:
- Higher affinity for dihydrofolate reductase than folic acid
- Inhibition of dihydrofolate formation
- Inhibition of purine/pyrimidine nucleotide synthesis
- Ultimately halt DNA and RNA synthesis

> > Ralitrexed, pemetrexed

> Nucleotide analogues

> > 5-fluorouracil: pyrimidine analogues - prevents thymidine formation & stops DNA synthesis

> > Mercaptourines: purine analogues which are converted into false nucleotides & disrupt purine nucleotide synthesis - may be incorporated in DNA, disrupting helix

> > Cytarabine (Ara-C): sugar moiety of cytidine is arabinosine rather than ribose (poses as 2’ deoxy); cellular activation to ara-CTP
> S-phase cell cycle specific, targets DNA replication and inhibits DNA polymerases; incorporation into DNA causes chain termination

> > Gemcitabine, fludarabine, capecitabine

66
Q

Describe cytotoxic antibiotics and describe their mechanism of action

A
  • Act mainly by a direct action on DNA as intercalators
  • Dactinomycin (isolated from Streptomyces)
    > Inserts itself into the minor groove in the DNA helix & binds
    > RNA polymerase function is disrupted
  • Doxorubicin (isolated from Streptomyces)
    > Inserts itself between base pairs
    > Local uncoiling leading to impaired DNA and RNA synthesis
    > Effective against many cancers
  • Microtubule inhibitors
    > Vinca alkaloids e.g. Vincristine, isolated from Madagascar periwinkles
    » Binds to microtubular protein blocking tubulin polymerisation
    » Blocks normal spindle formation & disrupts cell division
67
Q

Describe the types of steroid hormones and antagonists used in cancer treatment

A
  • Prednisone
    > Synthetic adrenocortical steroid hormone converted in the body to active form
  • Prendisolone
    > Suppresses lymphocyte growth
  • Tamoxifen
    > Antagonist of oestrogen receptor used in oestrogen-dependent breast cancers
  • Testosterone receptor antagonists
    > e.g. flutamide or bicalutamide. are used in the treatment of testosterone-dependent prostate cancers
  • Pituitary downregulators
    > LHRH agonists e.g. Prostap
    > Inhibit release of LH which normally stimulates testes to produce testosterone
68
Q

List 5 causes of menorrhagia

A
  • Fibroids (uterine leiomyomas)
  • Endometriosis
  • STIs e.g. chlamydia, gonorrhoea
  • PCOS (anovulatory menorrhagia)
  • Coagulation disorders e.g. von Willebrand disease
69
Q

Describe the diagnosis and symptoms of PCOS

A
  • Diagnosis
    > Total testosterone
    > Sex hormone binding globulin
    > Free androgen index calculation
    > Prolactin
    > TSH
    > LH:FSH ratio is 2:1
    > Ultrasound showing polycystic ovaries
  • Symptoms
    > Signs of hyperandrogenism e.g. hirsutism, acne
    > Obesity (signs of insulin resistance)
    > Oligomenorrhoea or amenorrhoea, anovulatory cycles
    > Infertility
    > Type II diabetes
70
Q

Describe the treatment of PCOS

A
  • Weight loss & encourage healthy lifestyle
  • Contraceptive pill (can induce regular periods)
  • Metformin
    > Drug for diabetes, can lower glucose levels
    > Increases sensitivity to insulin & induces ovulation
  • Fertility treatment: ovulation induction with clomiphene, IVF
  • FSH stimulation: with clomiphene or pulsatile LH releasing hormone analogues
  • Spironolactone: anti-androgen
  • Finasteride & flutamide: reduce hirsutism

Phase 3 (14 decks)

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