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FGU Flashcards

1
Q

Cervical polyp

A

benign overgrowth of connective tissue and epithelium of the cervix

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2
Q

What is the commonest kind of invasive breast cancer?

A

invasive ductal carcinoma

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3
Q

Her2 status

A

Refers to whether or not the carcinoma cells:

o EITHER over-express Her2 protein
o OR have HER2 gene amplification.

Without one of these the cancer is not a target for Herceptin

Her2 positive cancers have a worse prognosis

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4
Q

heterotopia

A

the presence of a particular tissue type at a non-physiological site

usually co-exists with original tissue in its correct anatomical location

e.g. ectopic breast tissue in the axilla

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5
Q

macromastia

A

Stromal overgrowth leading to excessive breast size

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6
Q

Acute mastitis

A

cellulitis associated with breast feeding

Skin fissuring may let bacteria in, and milk stasis favours growth, leading to infection of breast tissue

usually staphylococcus aureas

causes cardinal signs of inflammation + nipple discharge and fever

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7
Q

Idiopathic granulomatous mastitis

A

chronic inflammatory disease of the breast that can clinically mimic breast carcinoma

Distinct hard mass.

Do not excise

Exclude causes like sarcoidosis/TB

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8
Q

Characteristics of Fibrocystic change

A

most frequent benign breast condition

multifocal and bilateral
may cause breast tenderness

Cyclical Variation – Lumps tend to be bigger and more tender in latter half of menstrual cycle

Does not increase risk of cancer

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9
Q

Classification of Fibrocystic change

A

1) ‘non proliferative’ (with no significant excess risk of subsequent breast cancer)
2) ‘proliferative without atypia’, (up to 2-fold excess risk of breast cancer)
3) ‘proliferative with atypia’ (about 5-fold or more excess cancer risk, especially if there is a positive family history).

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10
Q

Adenosis

A

increase in glandular breast tissue

Microcalcifications may be observed on mammography
may cause a clinically suspicious mass.

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11
Q

Epithelial hyperplasia

A

Associated with increased cancer risk.

3 kinds:
1) Ductal hyperplasia of usual type

2) ‘Atypical ductal hyperplasia’ (ADH)
3) ductal carcinoma in situ (DCIS)

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12
Q

Lobular neoplasia

A

Associated with increased cancer risk.

  • atypical lobular hyperplasia (ALH)
  • lobular carcinoma in situ (LCIS)

The difference between ALH and LCIS is of extent and amount of cellular proliferation.

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13
Q

Radial scars

A

benign lesions

characterised by:
o a fibrotic and elastotic core
o trapped glands
o a pseudo-infiltrative appearance

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14
Q

Intraduct papilloma

A

benign

tumour of the epithelium lining the mammary ducts

under areola

causes bloody discharge from nipple

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15
Q

fibroadenomas

A

commonest in young women (teens - 30s).

Benign

hormone sensitive, and regresses after the menopause.

firm, non-tender, mobile lump

known as a “Breast mouse” because it is not tethered

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16
Q

Hamartoma of breast

A

rare, benign, tumour-like nodules composed of glandular, adipose and fibrous tissue

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17
Q

Risk factors for breast cancer

A 
o	earlier menarche
o	later menopause
o	being older at first pregnancy/childbirth
o	OCP use
o	HRT
o	Obesity
o	Tallness
o	denser breast tissue on mammography
o	alcohol
o	positive family history
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18
Q

Symptoms of possible breast cancer

A
  • A new lump or thickening in breast or axilla.
  • Altered shape, size or feel of the breast
  • pain (not often)
Skin changes: 
o	puckering 
o	dimpling
o	'peau d'orange' (skin oedema) 
o	Rash
o	Redness
o	feels different.

Nipple changes:
o tethering/inversion
o discharge
o eczema-like changes in Paget’s disease.

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19
Q

Investigation of breast abnormalities

A

Clinical examination - inspection in different positions, palpation.

Imaging - ultrasound, X-ray mammography, MRI

Fine needle aspiration cytology

Core biopsy

Excisional biopsy - diagnostic, therapeutic, or both

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20
Q

Treatment of breast cancer

A

Usually wide local excision followed by radiotherapy

Larger cancers may still require mastectomy to achieve clear margins

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21
Q

Spread of breast cancer

A

tends to metastasise to lymph nodes of the axilla by lymphatic spread

Staging the axilla is important for prognosis and treatment. This is done by sentinel node biopsy

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22
Q

which breast carcinomas are likely to respond to endocrine treatment?

A

ER/PR positive

About 80% breast cancers overexpress oestrogen receptor (ER) and progesterone receptor (PR).

• e.g. Tamoxifen for breast cancer that is ER positive (predominantly an ER antagonist)

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23
Q

Which drugs can be used to prevent oestrogen stimulation of tumour growth in breast cancer?

A

aromatase inhibitors

prevent conversion of (adrenal) androgens to oestrogen

NB: cause osteoporosis

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24
Q

Are ER, PR and Her2 status more important as prognostic or predictive factors?

A

important for predicting likely response to endocrine and Her2-targeting therapies

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25
Q

What are the most important prognostic factors for breast cancer?

A

Grade and Stage - tumour size and lymph node involvement

Ductal/no specific type tumours have worse prognosis

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26
Q

Which three histological properties is breast cancer grading based on?

A

Bloom & Richardson Grading

1) nuclear pleomorphism
2) the number of mitoses (mitotic rate)
3) the degree of gland formation by the cancer cells.

Grade 1 cancers - well differentiated and slow growing. Unlikely to benefit from chemotherapy

Grade 3 cancers - poorly differentiated and fast growing. more likely to be offered chemotherapy

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27
Q

Nottingham Prognostic Index

A

combines:
o Grade
o tumour size in cm
o stage

used to determine prognosis following surgery for breast cancer

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28
Q

Invasive ductal carcinoma (IDC)

A

most common type of breast cancer

usually has DCIS precursor

presents with palpable fibrous mass with sharp edges

Necrosis in the centre -> calcification

May present with paget’s disease of the nipple

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29
Q

Invasive lobular carcinoma (ILC)

A

characterised by loss of E-cadherin

usually LCIS precursor

bilateral presentation

less obvious mass.

Usually ER+

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30
Q

Ductal carcinoma in situ

A

o Malignant looking proliferation of epithelial cells within basement membrane.
o No extension into breast stroma
o No communication with blood vessels or lymphatics

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31
Q

ER+ cancers

A

‘Luminal A’ ER+ cancers tend to be low grade, less proliferative and have a better prognosis.

‘Luminal B’ ER+ cancers tend to be high grade, more proliferative and potentially do less well.

Remember: B is less good than A because A is a better grade

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32
Q

ER- cancers

A

three subtypes:
• normal breast like
• ‘HER2’
• basal-like - tend to be aggressive. Triple negative (no hormone receptors)

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33
Q

Premature Thelarche

A

premature breast development

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34
Q

Breast development

A

Breast tissue develops from the Mammary Ridge (Milk Line)
– pair of ectodermal thickenings
– spreads from the Axilla to the mid-thigh.
– appears in week 7

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35
Q

Effect of menstrual cycle on breast tissue

A
  • Proliferation in proliferative phase
  • Decreases in follicular phase
  • Myoepithelial changes & proliferation in Luteal phase

– Secretory changes in secretory phase

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36
Q

Effect of pregnancy on breast tissue

A

Early pregnancy - lobular enlargement & stromal depletion.

secretory change.

Post lactational involution when they stop breast feeding (takes about 3 months to complete).

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37
Q

Amastia

A

lack of breast tissue or no breast development

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38
Q

Polythelia

A

multiple small nipples

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39
Q

Polymasia

A

development of multiple small breasts along the milk line

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40
Q

Breast cancer screening

A

All women 50-70 years invited every 3 years

<50 the tissue is too dense

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41
Q

Phyllodes tumour

A

• Stromal Overgrowth – becomes more cellular

Can be:
o Benign – slight increased risk of return if removed
o Borderline – higher risk of return
o Malignant. Treat as Sarcoma

42
Q

Duct Ectasia

A

Also known as plasma cell mastitis

benign breast condition

lactiferous duct becomes blocked or clogged

may cause green discharge
• Linked to smoking
• Discharge tends to go away if person stops smoking

43
Q

(Traumatic) fat necrosis

A

benign breast condition

consists of fatty tissue that has been bruised, injured, or has died.

44
Q

Pathway of cancer development in the breast

A

Normal -> hyperplasia -> florid hyperplasia -> atypical hyperplasia -> malignancy

45
Q

Benign proliferative breast disease

A

group of noncancerous conditions that may increase the risk of developing breast cancer

o atypical ductal hyperplasia
o atypical lobular hyperplasia
o intraductal papillomas

46
Q

What non-breast malignancies can cause breast lumps?

A

lymphoma
sarcoma
angiosarcoma
melanoma

47
Q

what cell types line the ecto and endo cervix?

A

ectocervix - non keratinised stratified squamous

endocervix - columnar (glandular)

48
Q

which cervical cells are most commonly affected by HPV?

A

cells at the base of the squamous epithelium

HPV affects the way they divide

49
Q

How does HPV cause cervical cancer?

A

HPV is a potent carcinogen

it knocks out many of the tumour suppressor genes (e.g. p53 and p21) when the viral DNA is incorporated into the host’s DNA

This causes cells to continue to divide past the basal layer

50
Q

Which HPV strains are prevalent in Scotland?

A

HPV 16 and 18

51
Q

HPV can be grouped into low and high oncogenic risk. Which are high and which are low risk?

A
  • Low risk types e.g. 6 and 11 cause warts

* High-risk types 16 and 18 cause around 70% of cervical cancers.

52
Q

Risk factors for cervical cancer

A
  • HPV infection
  • Multiple sexual partners
  • Male partner with multiple previous/current partners
  • Young age at first intercourse
  • High parity
  • Persistent infection with high oncogenic risk HPV
  • Immunosuppression
  • Oral contraceptive pill
  • Smoking → interferes with the mechanism by which the body naturally eliminates HPV
53
Q

Cervical Intraepithelial Neoplasia (CIN)

A

a precancerous lesion

precursor to cervical squamous cell carcinoma

latent stage of the disease

54
Q

•CIN 1

A

one-third of the thickness of the surface layer is affected.

Most cases regress, 10% develop into CIN2 or 3

55
Q

CIN 2

A

two-thirds of the thickness of the surface layer is affected.

56
Q

CIN 3

A

full thickness of the surface layer is affected.

High grade dyskaryosis

CIN 3 is also known as carcinoma-in-situ.

57
Q

cervical screening

A

samples cells from the cervical transformation zone

designed to detect changes associated with HPV infection and CIN

o Age 25 to 50 three yearly
o Age 50 to 65 five yearly

designed to pick up squamous lesions

58
Q

Koilocytes

A

Squamous epithelial cells that have undergone structural changes as a result of HPV infection

perinuclear halo
Nuclear enlargement
Irregularity of the nuclear membrane contour
Hyperchromasia

59
Q

LLETZ biopsy

A

large loop excision of the transformation zone

The most commonly used treatment for removing abnormal cells from the cervix.

Can be carried out at the same time as a colposcopy

Removes area of the cervix where abnormal cells are.

Uses a thin wire loop heated with an electric current.

60
Q

HPV Vaccination

A

quadrivalent vaccine to cover against HPV 6, 11, 16 and 18

61
Q

Cervical Glandular Intraepithelial Neoplasia (cGIN )

A

pre-cancerous change involving the inner glandular cells of the cervix.

62
Q

Cervical Cancer Symptoms

A
  • Post coital bleeding.
  • Intermenstrual bleeding.
  • Irregular vaginal bleeding.
  • Pain.
  • None.
63
Q

atrophic vaginitis

A

thinning, drying and inflammation of the vaginal walls as a result of low oestrogen levels after menopause

discomfort, dyspareunia, and bleeding.

64
Q

Actinomyces

A
  • rare infectious bacterial disease

* Always associated with intrauterine coil

65
Q

characteristic histology of Herpes Simplex 2

A

intranuclear inclusions

66
Q

General Toxic Effects of Chemotherapy

A

Bone marrow suppression (anaemia, infections, bleeding)
hair loss
damage to GI epithelium
sterility

67
Q

cell-cycle specific drugs

A

• Drugs that are active only on dividing cells

68
Q

cell cycle-non specific drugs

A

• Drugs that are also active on resting cells

69
Q

Main classes of anticancer drugs

A

1) Cytotoxic antibiotics
2) Antimetabolites – alter DNA synthesis
3) Microtubule inhibitors
4) Steroid hormones/antagonists – specific tumours
5) Alkylating agents – act directly on DNA

CAMSA

70
Q

Mechanism of action: Alkylating Agents

A

Form covalent bonds with DNA

cross link with DNA so that the strands cannot separate, preventing transcription and translation

71
Q

Name 2 Alkylating Agents

A
  • Nitrogen mustards (Mechlorethamine)

* Cysplatin

72
Q

Mechanism of action: ANTIMETABOLITES

A

Antimetabolites interfere with nucleotide synthesis or DNA synthesis

  • Methotrexate
  • 5-fluorouracil
73
Q

Mechanism of action: Methotrexate

A
  • Causes inhibition of dihydrofolate formation
  • Inhibition of purine/pyrimidine nucleotide synthesis
  • Ultimately, halts DNA and RNA synthesis
74
Q

Mechanism of action: Cytotoxic Antibiotics

A

Act mainly by a direct action on DNA as intercalators

Insert into the DNA and bind so tightly that the DNA strands are unable to separate for DNA replication

Dactinomycin

75
Q

Mechanism of action: Microtubule inhibitors

A 
Vinca alkaloids (Vincristine)
•	Bind to microtubular protein
•	Block tubulin polymerisation
•	Block normal spindle formation 
•	Disrupt cell division
76
Q

Tamoxifen

A
  • Antagonist of oestrogen receptor

* used to treat breast cancers that are oestrogen dependent

77
Q

Salpingitis

A

part of the spectrum of pelvic inflammatory disease.

commonly an infective process –> bacteria

Usually an ascending infection from lower genital tract

Patients are typically systemically unwell

78
Q

Tubo-ovarian abscess

A

caused by Neisseria gonorrhoeae

one of the late complications of pelvic inflammatory disease (PID)

can be life-threatening if it ruptures

79
Q

Endometriosis

A

condition where the endometrium is found outside the womb, such as in the ovaries and fallopian tube

inflammatory disease

occurs in women of reproductive age

associated with:
o infertility
o dyspareunia
o chronic pelvic pain

80
Q

Most common Tubal malignancy

A

papillary serous carcinoma

Often have abnormalities in BRCA1 gene

81
Q

“STIC” = Serous Tubal Intraepithelial Carcinoma

A

Dysplasia in the lining of the fallopian tube
carcinoma in situ
precursor for high grade serous carcinoma

82
Q

PCOS

A

Over-production of androgens by multiple cystic follicles in the ovaries
o LH high, FSH low. (>2:1 ratio)

Presentation: 
o	Oligomenorrhea
o	Hirsutism
o	Infertility
o	obesity

• Metabolic syndrome - Insulin resistance, may develop type 2 diabetes

83
Q

What 3 cell types can ovarian neoplasms arise from?

A

1) surface epithelium
2) germ cells
3) sex cord/stromal cells

84
Q

Risk factors for epithelial ovarian cancers

A

o nulliparity
o family history

BRCA1 and BRCA2 gene mutations

85
Q

Types of malignant ovarian epithelial tumours

A 
o	cystic (cystadenocarcinoma) 
o	solid (adenocarcinoma)

high grade serous are most common (p53/BRCA1 mutation)

some ‘ovarian’ carcinomas are now thought to be of endometrial or Fallopian tube origin with spread to the ovary

86
Q

Endometrioma

A

“chocolate cyst”

subtype of endometriosis
presence of endometrial tissue in/on the ovary

thick, old blood that appears as a brown fluid

87
Q

What is the most common type of ovarian tumour?

A

Serous ovarian tumours

Can be benign or malignant

Usually p53/BRCA 1 mutations

  • Thin walled
  • Contain this watery serous fluid
88
Q

Histological features of high grade serous carcinoma

A
  • mitotic figures visible
  • very prominent nucleoli
  • invading into surrounding stroma
89
Q

Krukenberg tumor

A

malignancy in the ovary that has metastasized from a primary site, classically the gastrointestinal tract (gives rise to mucinous tumours)

NB: Large unilateral tumours are more likely to be primary tumours of the ovary

90
Q

dermoid cysts

A

mature cystic teratomas

ovarian germ cell tumours

NB: testicular germ cell tumours are almost always malignant wheareas ovarian germ cell tumours are almost always benign

91
Q

What is the triple assessment of breast?

A

Examination (physical + bloods)
Imaging
Biopsy

92
Q

DCIS

A

from ductal hyperplasia

cheesy discharge

93
Q

Which blood marker is sensitive for ovarian pathology?

A

Ca125

NB: not specific. Can be raised in other malignancies

94
Q

What is the main radiological investigation in ovarian pathology?

A

ultrasound scan

95
Q

What is the function of application of 5% acetic acid during colposcopy?

A

causes an ‘acetowhite’ colour change of the cervical squamous epithelium

This helps the colposcopist to identify areas of altered squamous epithelium and to target biopsies appropriately

96
Q

Where are mitoses (dividing cells) most likely to be seen in normal cervical stratified squamous epithelium?

A

Just above the basal layer (in the proliferative zone)

The basal layer itself includes stem cells and does not proliferate very rapidly.

97
Q

What is described as having a characteristic ‘watered silk’ appearance?

A

uterine fibroids (leiomyomas)

= a benign smooth muscle tumour

98
Q

What’s the correct term for a malignant smooth muscle tumour?

A

Leiomyosarcoma

99
Q

Neoplasm:

A

an abnormal growth of cells (usually excessive), may or may not be in response to a stimulus

Can be benign or malignant

100
Q

A woman presents with a tumour on her ovary. Immunocytochemical tests indicate that it has a gastrointestinal phenotype. Is this tumour a metastatic deposit?

A

Not necessarily

ovarian mucinous tumours can have a GI phenotype, this is not necessarily a metastasis

more likely to be a metastasis if bilateral

101
Q

What is the most common metastatic cancer to the breast?

A

melanoma

J3 (18 decks)

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