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Phase 3 > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What are significant developmental abnormalities involving the breasts?

A
  • Ectopic breast tissue is the most common abnormality, most often on the milk line between axilla and the groin
  • Nipple-areolar and glandular tissue may all be present but there may be glandular tissue without an obvious nipple or a nipple with little glandular development
  • Breast hypoplasia can occur, associated with many syndromes (CAH)
  • Nipple inversion is common and usually normal, new can however be a sign of benign or malignant disease
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2
Q

What are general inflammatory conditions affecting the breast?

A
  • May be infective or non-infective
  • Granulomatous inflammation of the breast tissue can occur in systemic diseases (sarcoid), and infections (TB)
  • Foreign body reactions around breast implants, and reactions to silicone leakage after implant rupture
  • Recurrent subareolar abscesses may be associated with maxillary fistula and smoking
  • Fat necrosis may follow trauma and is a benign process, but biopsy may be required to rule out cancer
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3
Q

What is idiopathic granulomatous mastitis?

A

A lobule centred, non-necrotising granulomatous inflammatory process with a tendency to recurrent after excision

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4
Q

What is acute mastitis?

A
  • Acute mastitis is a cellulitis associated with breast feeding
    • skin fissuring may let bacteria in, and milk stasis favour their growth, leading to infection of breast tissue
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5
Q

What is periductal mastitis/ductal ectasia?

A
  • Dilation of central lactiferous ducts, periductal chronic inflammation, and scarring
  • Often asymptomatic but there may be discomfort, a mass, nipple retraction or inversion
  • Calcified luminal secretions may be seen on mammogram
  • May progress to squamous metaplasia of lactiferous duct
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6
Q

What is fibrocystic change?

A
  • The most frequent benign breast condition, tends to be multifocal and bilateral and may cause breast tenderness and nodularity
  • Spectrum of change includes small and large cysts, increased amounts of glandular tissue, increased fibrous stroma, epithelial hyperplasia (without atypia, occasionally with)
  • Apocrine metaplasia of cyst epithelium is frequent
  • Solitary papillomas, papillomatosis and radial scars are also part of the wider spectrum of fibrocystic change
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7
Q

What is an intraduct papilloma?

A
  • Benign tumour of the epithelium lining the mammary ducts
  • Solitary central papillomas are thought to be innocuous if there is no epithelial atypia
  • Papillomatosis (multiple) is thought to be slightly more likely to be associated with malignancy elsewhere in the same or even contralateral breast
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8
Q

How is fibrocystic change classified?

A
  • Non proliferative: with no excess risk of subsequent BCR
  • Proliferative without atypia: up to 2-fold excess risk of BCR
  • Proliferative with atypia: about 5x the risk, especially with FH
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9
Q

What are specific variants in fibrocystic change?

A
  • Adenosis refers to an increase in glandular breast tissue
  • Specific types include sclerosing adenosine, which is a benign proliferation of distorted glandular tissue and stroma
  • Microcalcifications may be observed on mammography
  • Apocrine metaplasia is recognised by large, rounded epithelial cells with copious granular eosinophilic cytoplasm and characteristic apical projections
  • Radial scars are benign lesions characterised by a fibrotic and elastic core, trapped glands and a pseudo-infiltrative appearance
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10
Q

Describe epithelial hyperplasia:

A
  • Associated with increased cancer risk
  • Different patterns recognised as ductal or lobular
  • Ductal hyperplasia may be mild, moderate or florid with a mixture of cell types
  • Atypical ductal hyperplasia (ADH) is associated with microcalcifications and has features in common with low grade ductal carcinoma in situ
  • Lobular neoplasia includes atypical lobular hyperplasia and lobular carcinoma in situ; difference is extent and amount of cellular proliferation
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11
Q

What are columnar cell lesions?

A
  • Often associated with micro calcifications

- Columnar cell change and columnar cell hyperplasia without and with atypia

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12
Q

Describe fibroademona of the breast:

A
  • Common (25% of asymptomatic women)
  • Overgrowth of epithelium and stroma, resembling a giant lobule
  • Benign neoplasm, hormone sensitive, regress after menopause
  • Firm, non-tender, mobile and usually < 25-30mm
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13
Q

Desciribe Phyollodes tumour:

A
  • Overgrowth of epithelium and stroma but with increased stromal cellularity, mitotic activity, cytological atypia and an infiltrative border
  • Tendency to local recurrence and can become malignant
  • Requires surgical excision
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14
Q

What factors pre-dispose to BCR?

A
  • Increasing risk with age
  • Earlier menarche and later menopause
  • Older age at first pregnancy
  • OC use
  • HRT
  • Obesity and tall height
  • Denser breast tissue
  • Alcohol
  • Positive FH
  • Uncommon BCR genetic syndromes (BRCA1,2, p53)
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15
Q

How are breast abnormalities investigated?

A
  • Clinical exam
  • Imaging: Xray mammography, ultrasound, MRI
  • FNA cytology with microscopy of cells recovered
  • Core biopsy (often guided by imaging) with microscopy of tissue sections
  • Excision biopsy: diagnostic, therapeutic or both
  • Screening
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16
Q

What are signs of BCR?

A
  • New lump or thickening in breast or axilla
  • Altered shape, size or feel of the breast, pain
  • Skin changes; puckering, dimpling, skin oedema, rash, redness, feels different
  • Nipple changes; tethering/inversion, discharge, eczema-like changes in Paget’s disease
  • Rarely, widespread inflammation, redness, pain in inflammatory cancer can stimulate infection
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17
Q

Describe steroid hormone receptors in BCR:

A
  • ~80% BCRs overexpress oestrogen receptor and progesterone receptor
  • ER/PR positive carcinomas are likely to respond to endocrine treatment eg with tamoxifen which in breast is predominantly an ER antagonist, or aromatase inhibitors
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18
Q

Describe HER2 positive cancers:

A
  • Over-expression of HER2 has worse prognosis than other BCRs but treatment with monoclonal antibodies is effective
  • Adjuvant therapy can reduce risk of relapse
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19
Q

Describe Nottingham prognostic index:

A
  • Combines grade (based on histological properties, as well as differentiation and growth), tumour size in cm and stage into a numerical prognostic index
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20
Q

How is BCR morphologically graded?

A
  • BCR grading is based on three histological properties:
    1. Nuclear pleomorphism
    2. Number of mitosis per mm*2
    3. Degree of gland formation by the cancer cells
  • Grade 1 are well differentiated and slow growing while grade 3 are poorly differentiated and fast growing
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21
Q

How is BCR morphologically and molecularly classified?

A
  • Molecularly by presence or absence of ER, PR, Her 2 and androgen receptor (AR)
    • ER positive split into luminal A and B
    • ER negative split into normal breast like, HER2 and basal-like
  • Morphologically major divisions are invasive ductal carcinoma (IDC) and invasive lobular carcinoma (ILC)
    • lobular can mean ‘having lost E-cadherin’
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22
Q

Describe ductal/lobular carcinoma in situ:

A
  • Malignant looking proliferation of epithelial cells within basement membrane
  • No extension into breast stroma
  • No communication with blood vessels or lymphatics
  • No possibility of metastases
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23
Q

Describe changes in the cervix at puberty and menopause:

A
  • Prior to puberty the ectocervix is covered by non-keratinising stratified squamous epithelium and the endocervix is lined by columnar (glandular) epithelium
  • Squamo-columnar junction is everted into the vagina and the squamous epithelium adapts to the vaginal environment by squamous metaplasia in the ‘transformation’ zone
  • Changes are reversed at menopause
  • This zone of unstable differentiation is where most cervical neoplasia develop
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24
Q

Describe the effect of HPV on the lower female genital tract:

A
  • More than 99% of cervical carcinomas are associated with HPV infection
  • Early genes E1 to 7 interact with intracellular molecules to interfere with cell proliferation machinery to replicate the virus
  • Late genes L1,2 encode capsid proteins. Disruption of cell cycle checkpoints may contribute to accumulation of oncogenic mutations and carcinogenesis
  • Causes dyskaryosis suggestive of cervical intraepithelial neoplasia (CIN)
25
Q

Describe squamous intraepithelial neoplasia:

A
  • Invasive squamous carcinoma of the cervix almost always develops from pre-existing CIN, but not all CIN will become squamous cancer
  • CIN II and III are more likely to progress than CIN I
26
Q

Describe vulvar cancers:

A
  • SCC associated with VIN
    • females less than 60
    • associated with high incidence of lower genital tract neoplasia particularly CIN and invasive cervical cancer
    • usually related to high risk type HPV 16/18
    • warty or basaloid cancers
  • SCC associated with dermatoses
    • most over 60/70
    • well differentiated and keratinising
    • not associated with HPV or VIN
    • adjacent squamous hyperplasia and/or lichen sclerosis common
27
Q

Describe vulvar cancers:

A
  • SCC associated with VIN
    • females less than 60
    • associated with high incidence of lower genital tract neoplasia particularly CIN and invasive cervical cancer
    • usually related to high risk type HPV 16/18
    • warty or basaloid cancers
  • SCC associated with dermatoses
    • most over 60/70
    • well differentiated and keratinising
    • not associated with HPV or VIN
    • adjacent squamous hyperplasia and/or lichen sclerosus common
28
Q

What is the normal structure of the fallopian tube?

A
  • Lined by ciliated columnar epithelium
  • Complex plicae
  • Layers of smooth muscle
  • Peritoneum
29
Q

What are the main pathologies of the fallopian tubes?

A
  • Salpingitis
  • Ectopic pregnancy
  • Endometriosis (tubal involvement can compromise tube function)
  • Tubal malignancies
  • Serous tubal intraepithelial carcinoma (STIC)
30
Q

Describe salpingitis and its complications:

A
  • Part of spectrum of pelvic inflammatory disease
  • Most commonly infective (chlamydia, mycoplasma, gonorrhoea)
  • Usually considered to be ascending infection
  • Symptoms include fever, lower abdominal or pelvic pain and pelvic masses if tubes distended with exudate or secretions
  • Complications include adherence of tube to ovary, causing tubo-ovarian abscess
31
Q

Describe salpingitis caused adherence of FT and risk with ectopic pregnancy:

A
  • Adhesions involving tubal plicae increase risk of tubal ectopic pregnancy
  • Damage or obstruction of tube lumen may produce infertility which may not be easy to treat
  • Ruptured tubal ectopic pregnancy can be potentially life-threatening
32
Q

Describe tubal malignancies:

A
  • Primary adenocarcinomas involving and identified as arising from the FTs alone are rare
    • the most common is papillary serous carcinoma
    • endometrioid carcinomas are also seen
  • FT tube carcinomas occur in women with BRCA1 mutations (some occur after prophylactic oophorectomies)
  • FT carcinomas often involve momentum and peritoneal cavity at time of presentation
33
Q

Describe ‘STIC’:

A
  • Recent concept of serous tubal intraepithelial carcinoma
  • Abnormal epithelium in the distal fallopian tube
  • Lined by basement membrane so no carcinoma in situ
  • Nuclear atypia clearly seen, and is likely a precursor for high grade serous carcinoma
  • Similar mutations to invasive tumour, including p53
34
Q

Describe the normal structure of the ovaries:

A
  • Flat surface epithelium
  • Cortex:
    • compact ovarian stroma
    • small functional cysts
    • germ cells
  • Medulla:
    • hilus cells
    • vessels
    • nerves
35
Q

Describe non-neoplastic cysts (such as polycystic ovaries):

A
  • Symptoms of polycystic ovaries include (usually after menarche):
    • oligomenorrhoea
    • hirsutism
    • infertility
    • obesity
    • over-production of androgens by multiple cystic follicles in the ovaries
    • LH high, FSH low
  • Enlarged ovaries with many subcortical cysts seen
    • Thickened, fibrotic outer surface over cysts lined by granulose cells with a hypertrophic and hyperplastic lutenised theca interna
    • Absence of corpora lutea and corpora albicantes
36
Q

Describe ovarian neoplasms:

A
  • Tumours related to three cells that make up ovary:
    1 surface (coelomic) epithelium
    2 germ cells
    3 sex cord/stromal cells
  • Benign surface epithelial tumours are usually cystic (cyst adenoma) with/out a solid stroll component
  • Malignant epithelial tumours may be cystic or solid
  • 95% of germ cell tumours are mature cystic teratomas, mostly benign
  • Sex cord tumours can be granulosa and theca cell tumours
    • granulose usually occur in postmenopausal women and are not rare
    • ovarian fibromas and thecomas are usually benign and not rare
37
Q

What are the clinical correlations for all ovarian tumours?

A
  • Often asymptomatic until well advanced
  • Clinical presentations often similar despite biological diversity: local pressure symptoms (pain, GI complaints, urinary frequency)
  • Sometimes they become twisted on their pedicles (torsion) producing severe abdominal pain
38
Q

How else can surface epithelial tumours be described?

A
  • Intermediate, borderline category referred to as low malignant potential
  • Carcinomas may be high grade serous, endometrioid, clear-cell, low grade serous or mucinous
    • HGSC are though to arise from epithelial precursor lesions in the ovarian end of the FTs
    • Endometrioid and clear cell carcinomas probably arise from ovarian endometriosis
39
Q

Describe endometriosis:

A
  • The presence of endometrial tissue outside the uterus
  • Common sites of endometriosis include ovaries, peritoneal surfaces, large and small bowel, appendix, mucosa of cervix, vagina and fallopian tubes and laparotomy scars
  • Clinical symptoms include dysmenorrhoea, pelvic pain and infertility
  • Pathogenesis is by metastatic theory (retrograde menstruation) or metaplastic theory (arising from coelomic epithelium)
40
Q

Describe endometrial polyps:

A
  • Exophytic masses of variable size which project into the endometrial cavity
  • Associated with tamoxifen in some cases
  • Appearance:
    • Microscopically haphazardly arranged glands with preservation of a low gland to stroma ratio
    • Often thick walled blood vessels and fibrous stroma
    • Glands are usually inactive but can also show proliferation, secretory changes or metaplasia
  • Can present with abnormal bleeding and be treated via hysteroscope
41
Q

What is adenomyosis?

A

The presence of endometrial tissue within the myometrium

42
Q

Describe endometrial hyperplasia and adenocarcinoma:

A
  • Symptoms: usually postmenopausal bleeding
  • Histologically characterised by an increase in the gland to stroma ratio, and can be seen with or without cytological atypia
  • Hyperplasia is known precursor of adenocarcinoma
  • Management:
    • hyperplasia: progesterone therapy or hysterectomy
    • adenocarcinoma: hysterectomy with subsequent management depending on tumour grade and stage
43
Q

What causes endometrial hyperplasia and adenocarcinoma?

A
  • Associated with prolonged oestrogen stimulation of the endometrium
  • Possible underlying causes include:
    • anovulatory cycles
    • endogenous sources of oestrogen (obesity, PCOS, oestrogen secreting ovarian tumours)
    • exogenous sources of oestrogen such as oestrogen only HRT
44
Q

Describe leiomyoma:

A
  • Benign smooth muscle tumour of the myometrium
  • Very common- at least 25% of women, mostly of reproductive age, incidence is over 70% by age 50
  • May be single or multiple
  • Symptoms:
    • asymptomatic
    • abnormal bleeding
    • urinary frequency if large
    • impaired fertility
45
Q

Describe the pathology and management of leiomyoma:

A

Pathology:
- sharpy demarcated round grey-white tumours with a whorled cut surface, very variable in size
- microscopically resemble normal smooth muscle
Management:
- varies depending on number, seize and symptoms
- Medical; progesterone secreting IUS, hormonal therapies, transexamic acid, GnRH agonists
- Surgical; uterine artery embolisation, myomectomy, hysterectomy

46
Q

Describe leiomyosarcoma:

A
  • Uncommon malignant smooth muscle tumour of the myometrium (commonest uterine sarcoma)
  • Peak incidence age is 40-60 years, can be pre or post menopausal
  • Symptoms initially none, then bleeding or pain
  • Pathology
    • macro: bulky invasive masses or polypoid necrosis, haemorrhage and variable cut surface
    • micro: overt cytological atypia, necrosis, mitotic activity, infiltrative margin
47
Q

Describe endometrial stromal sarcoma:

A
  • A group of tumours of the endometrial stroma
  • Can be low grade (common) or high grade (rare)
  • Both have diffusely infiltrative ‘worm like’ growth pattern macroscopically
  • Microscopy
    • low grade tumour cells resemble cells of proliferating endometrial stroma, with mitoses
48
Q

What is gestational trophoblastic disease?

A

An umbrella term for several conditions including hydatidiform moles (partial and complete) and malignant tumours including choriocarcinoma

49
Q

What is partial mole?

A
  • Fertilisation of one egg by two sperm resulting in a triploid karyotype
  • Microscopy shows oedematous villi and subtle trophoblast proliferation
  • Risk of invasive mole which invades and destroys the uterus
50
Q

What is complete mole?

A
  • Fertilisation of an egg with no genetic material, usually by one sperm which duplicates its chromosomal material
  • Diploid karyotype, usually 46 XX
  • Microscopy shows enlarged oedematous villi with central cisterns and circumferential trophoblast proliferation
  • Carries a 10% risk of invasive mole and a 2.5% risk of choriocarcinoma
51
Q

What are the main classes of chemotherapy drugs?

A
  • Alkylating agents
  • Antimetabolites
  • Cytotoxic antibiotics
  • Microtubule inhibitors
  • Steroid hormones and antagonists
52
Q

Describe alkylating agents:

A 
Function
- Form covalent bonds with DNA
- Interfere with both transcription and replication
- Most alkylating agents have two reactive groups
- Allow the drug to cross-link
  - within one strand of DNA
  - across the two strands of DNA
Drugs
- Nitrogen mustards
- Cysplatin
- Temozolomide
- Lomustine (can penetrate brain)
- Busulphan ('selective' effect on bone marrow)
53
Q

Describe cyclophosphamide:

A
  • A prodrug that requires activation by phosphoramidase
  • High phosphoramidase activity in some tumours
  • Much less toxic than other nitrogen mustards
  • Aldehyde dehydrogenase (ALDH) protects against the toxicity of the drug
  • Used to treat many cancers
54
Q

Describe antimetabolites types:

A 
Nucelotide synthesis: anti-folates
- methotrexate
- ralitrexed
- pemetrexed
Nucleotide analogues
- 5-fluorouracil
- Cytarabine
- Gemcitabine
- Fludarabine
- Capectabine
55
Q

How do antimetabolites act?

A

Methotrexate:
- higher affinity for dihydrofolate reductase than folic acid
- inhibition of dihydrofolate formation
- inhibition of purine/pyrimidine nucleotide synthesis
- ultimately halt to DNA and RNA synthesis
Fluoro-uracil:
- prevents thymidine formation
- stops DNA synthesis
Mercaptopurines
- converted into false nucleotides
- disrupts purine nucleotide synthesis
- may be incorporated into DNA, disrupting helix

56
Q

How does cytarabine act?

A
  • Sugar moiety of cytidine is arabinosine rather than ribose
  • Cellular activation to ara-CTP
  • S-phase cell cycle specific
  • Inhibits DNA polymerases
  • Incorporation into DNA causes chain termination
57
Q

How do cytotoxic antibiotics work?

A

Act mainly by direction action on DNA as intercalators

  • Dactinomycin
    • inserts itself into the minor groove in the DNA helix
    • RNA polymerase function is disrupted
  • Doxorubicin
    • inserts itself between base pairs
    • binds to the sugar-phosphate DNA backbone
    • local uncoiling
    • impaired DNA and RNA synthesis
  • Vincristine
    • bind to micro tubular protein, block tubulin polymerisation and normal spindle formation and disrupt cell division
58
Q

How do steroid hormones work?

A

Work on tumours that are responsive to a specific hormone which makes it regress

  • Tamoxifen (antagonist of oestrogen receptor)
    • treats oestrogen dependent breast cancers
  • In prostate cancer treatment can be testosterone receptor antagonists and pituitary down regulators

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