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3rd Year > Case 13 > Flashcards

Case 13 Flashcards

0
Q

Typical sequence leading to neoplasia

A

Mutation inactivates tumour suppressor
Cells proliferate
Mutation inactivates DNA repair genes
Mutation of proto-onco gene creates oncogene
Mutations inactivate several more tumour suppresor genes

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1
Q

What are the molecular hallmarks of cancer?

A 
Provide own growth signals
Insensitive to stop signals
Unlimited proliferative potential
Avoidance of apoptosis
Sustained angiogenesis
Tissue invasion and metastatic ability
Unstable genome
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2
Q

Multistep, multigene model of tumorigenesis

A

Mut. 1: cell seems normal but is predisposed to excessive proliferation
Mut. 2: cell proliferates too much but is otherwise normal
Mut.3: cell proliferates more rapidly and undergoes structural changes
Mut. 4: cell proliferates uncontrollably and looks obviously deranged

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3
Q

Categories of cancer risk factors

A

Genetics
Chemicals
Viruses or bacteria
Radiation

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4
Q

Name 5 cancer viruses and their associated malignancies

A 
EBV - Burkitt's lymphoma
HPV - cervical carcinoma
HBV - HCC
HTLV1- Adult T cell leukaemia
HHV8 - Kaposi's sarcoma
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5
Q

Role of E7 in cervical carcinoma

A

Overrides G1/S restriction point
Rb normally binds E2F transcription factors, preventing promoter DNA regions from being switched on
E7 binds Rb, allowing excessive E2F to bind to DNA promoter sequences and driving the cell into the S phase

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6
Q

Role of E6 in cervical cancer

A

Inactivates p53 tumour suppressor

E6 causes ubiqitination of p53, causing its breakdown

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7
Q

Role of p53

A

DNA repair
Arrests abnormal cells at the G1/S checkpoint
Initiates apoptosis

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8
Q

Establishing a link between a virus and a cancer

A

Cancer is prevalent in viral prevalent regions
Individuals with cancer have evidence of persistent viral infection
Viral cell tropism is thecame as the cancer cell of origin
Viral nucleic acids are present in tumour cells
Incidence of cancer reduced by infection control measures

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9
Q

Role of viruses in oncogenesis

A

Inactivation of tumour suppressor proteins
Trans-activation of cellular proteins by viral TFs
Action of viral oncogenes

Failure of immune surveillance

Cofactors

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10
Q

HPV mucosal subtypes

A

6 and 11

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11
Q

HPV common cutaneous subtypes

A

1,2,3,4,5,8

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12
Q

Which HPV subtypes are associated with laryngeal papillomas?

A

6 and 11

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13
Q

Risk factors in multifactorial genetic disorders

A

Baseline risk
Number of affected relatives, esp FDRs
Age of onset in affected relatives
Predisposing environmental factors

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14
Q

Knudson’s 2 hit hypothesis

A

AD inheritance of one mutated TS/DNA repair allele
Born with one functional allele
Relevant protein still produced at 50% of normal levels, sufficient for function
2nd hit occurs with somatic mutation causing loss of tumour suppression/DNA repair

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15
Q

Loss of tumour suppressor genes may be due to…

A

Loss of function mutation

Epigenetic silencing

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16
Q

What is the role of the BRCA gene mutations and what is their inheritance?

A

Role in DNA repair

AD inheritance

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17
Q

Distinguishing hereditary from multifactorial breast cancer

A 
Suspect hereditary if:
Pedigree suggests AD pattern
Early onset
Muftifocal/bilateral disease
Male
Ovarian CA
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18
Q

List 5 signalling modalities present int he female genital tract and give an example of each.

A

Endocrine - FSH acts on GCs to increase aromatase activity

Paracrine - inhibin from GCs acts on theca interna, assists LH in stimulating androstenedione synthesis

Autocrine - activin from GCs increases GC FSH receptors

Synaptic - parasympathetic stimulation results in arousal

Cell-cell - gap junctions between GCs and oocyte

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19
Q

Histological components of the ovarian cortex

A 
Lined by germinal epithelium
Resting follicles
Maturing/developing follicles
Atretic follicles
Fibrous stroma
Corpus luteum (after ovulation)
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20
Q

Histological components of the ovarian medulla

A

Connective tissue
Interstitial cells
Nerves
Blood vessels

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21
Q

What stage of oocyte do primordial and primary (pre-antral) follicles contain?

A

Primary oocytes, arrested in prophase 1

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22
Q

Functions of the ovary

A

Production of the female gamete
Secretion of oestrogen and progesterone
Regulation of postnatal growth of reproductive organs
Development of secondary sexual characteristics

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23
Q

Phases of the ovarian cycle

A

Follicular
Ovulatory
Luteal

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24
Q

Phases of the uterine cycle

A

Menstrual
Proliferative
Secretory
Ischaemic

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25
Q

Histological appearance of primordial follicles

A

Squamous, flattened granulosa cells

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26
Q

Histological appearance of primary follicles

A

Cuboidal granulosa cells, unilayer

Zona pellucida begins to form

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27
Q

Histological appearance of early secondary follicles

A

Stratified cuboidal granulosa cells
Zona pellucida fully assembled
Theca differentiating

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28
Q

Histological appearance of pre antral secondary follicle

A

Well differentiated theca

Beginnings of antrum are seen as liquor-filled spaces between granulosa cells

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29
Q

Histological appearance of tertiary/antral/Graafian follicle

A

Antrum
Cumulus oophorus
Corona radiata

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30
Q

Follicular events following ovulation

A

LH stimulates fibroblasts at the stigma to degrade the theca externa

Mural granulosa layer folds inwards
Basement membrane breaks down, blood vessels from theca interna invade folding granulosa layer

Antral cavity fills with blood

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31
Q

Histological appearance of atretic follicles

A

Thick, folded basement membrane
Delaminating granulosa cells
Invading macrophages

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32
Q

Development of the corpus luteum

A

Breakdown of basal lamina
Invasion of blood vessels
Transient corpus haemorrhagicum invaded by blood vessels, fibroblasts and collagen fibres
Mural GCs transform into granulosa lutein cells
Theca interna cells become theca lutein cells

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33
Q

Characteristics of steroid secreting cells

A

Lipid droplets
Well developed smooth ER
Mitochondria with tubular cristae

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34
Q

Histological appearance of the corpus albicans

A

Fibrous ovarian stroma with blood vessels

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35
Q

Theca interna cell functioning

A

LH stimulation causes uptake of cholesterol from the blood and steroidogenesis
The steroid products are progesterone and androstenedione
Androstenedione is translocated to the granulosa cells for aromatisation

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36
Q

Granulosa lutein cell functioning

A

Under the control of both LH and FSH
Store cholesterol for progesterone synthesis
Convert androstenedione to estradiol

37
Q

Granulosa cell functioning

A

FSH stimulates GC proliferation and the production of oestrogen and progesterone
Activin, placental lactogens and prolactin enhance FSH sensitivity
FSH stimulates inhibin secretion which enhances theca lutein sensitivity to LH

38
Q

When do GCs acquire LH receptors?

A

Graafian follicle stage

39
Q

What maintains the oocyte in arrested prophase 1?

A

Oocyte maturation inhibiting factor

40
Q

When is the first polar body formed and where is it found?

A

Following completion of meiosis 1 just before ovulation.

Found in the perivitilline space

41
Q

What type of molecule makes up the zona pellucida?

A

Glycoproteins

42
Q

Effects of the LH surge on the Graafian follicle

A

Halts oestrogen production
Initiates second meiotic division
Local prostaglandin production causes vascular follicular swelling and proteolytic enzyme activity
After ovulation,causes luteinisation

43
Q

Histology: uterine proliferative phase

A

Endometrium increases in thickness
Straight tubular glands become tortuous
Cells change from low to tall columnar with mitotic figures
Mesenchymal mitotic figures, slight oedema

44
Q

Histology: uterine secretory phase

A

Endometrial thickness increases further

Glands become more tortuous, glycogen/glycoprotein secretions visible in lumen

Tall columnar cells with basal glycogen accumulation/displaced nucleus

Stroma: fewer mitotic figures, cells enlarge, increasing oedema, lymphocytic infiltrate

45
Q

Histology: endocervix

A

Large branched tubular glands
Columnar mucous secreting epithelium with some cilia
Fibroelastic stroma

46
Q

Histology: ectocervix

A

Stratified squamous epithelium

47
Q

Potential risks: cervical transformation zone

A

Early puberty - infections
Nabothian cysts
Dysplasia
Carcinoma

48
Q

Pap cytology

A

Acidophilic cells: fully differentiated, from superficial layer, pyknotic nuclei. Abundant at ovulation

Basophilic cells: from deeper layers, plumper normal-looking nuclei. Abundant postovulatory

49
Q

Anatomic regions of the uterine tube

A

Infundibulum
Ampulla
Isthmus
Intramural

50
Q

Uterine tube histology

A

Epithelium: columnar cells - cilliated cells and non-cilliated peg cells with apical microvilli
Lamina propria
Muscle layer: inner circular outer longitudinal
Mesothelial serosa

51
Q

Characteristic sign of HPV on pap smear

A

Koilocytosis

52
Q

Structure of the vagina

A

Mucosa: stratified squamous epithelium with lamina propria

Muscularis layer with circular and longitudinal layers

Outer dense adventitial layer

Mucosa,epr moist by endocervical and Bartholin’s glands in lower vagina.

53
Q

Where are Skene’s glands found?

A

Adjacent to the urethral meatus

54
Q

What constitutes an unnatural death?

A

Application of force, physical, chemical or other factors
Act of omission or comission
Procedure-related death
Unexpected/unexplained death

55
Q

Pathogenesis of TB in the female genital tract

A

Haematogenous spread to the uterine tubes
Chronic inflammation with granulomas and caseous necrosis
Direct spread to the uterus causes tuberculous endometritis

56
Q

Commonest site of extrauterine pregnancy

A

Uterine tube

57
Q

Causes of tubal ectopic pregnancy

A

Partial obstruction following salpingitis

Delayed pickup of the ovum by the fimbriae

58
Q

Major complication of a tubal ectopic

A

Rupture and haemorrhage due to trophoblastic invasion of the wall of the uterine tube

59
Q

Ectopic endometrial tissue may arise due to…

A 
Retrograde spread during menstruation
Implantation during c/s
Metaplasia
Lymphatic spread involving nodes
Blood spread
60
Q

Endometriosis sites

A 
Ovary, tubes, pouch of Douglas
GIT (recto-sigmoid)
Umbilicus and surgical scars 
Pelvic lymph nodes
Distant sites - lungs
61
Q

Macroscopic appearance endometeiosis

A

“Chocolate cysts” with fibrosis due to cyclical haemorrhage

62
Q

Microscopic appearance endometriosis

A

Endometrial glands plus steoma

Haemosiderin-laden macrophages

63
Q

Complications of endometriosis

A

Infertility
Adhesions
Intermittent intestinal obstruction
Endometrioid carcinoma

64
Q

Cervical CA epidemiology

A

Commonest non-cutaneous malignancy in SA
Age 20-80 (commonest 35-50)
Regarded as STD

65
Q

Risk factors for cervical cancer

A 
High risk HPV infection
Promiscuity, early debut, parity, STIs
Cigarette smoking
Oral contraceptive
Long interval since last pap smear
Low SES
66
Q

Cervical biopsy grading

A

CIN 1, 2 and 3 (British system)

67
Q

Cervical cytology grading

A

LSIL/HSIL (Bethesda system)

68
Q

Macroscopic appearance of cervical carcinoma

A

Ulcerating, exophytic or nodular

69
Q

Microscopic appearance of cervical carcinoma

A

Squamous carcinoma with or without keratin

70
Q

Adenocarcinoma

A

Much less common
Some related to HPV
Age 30-60

71
Q

Staging cervical carcinoma

A

FIGO staging
0. Carcinoma in situ

  1. Carcinoma confined to the cervix visible microscopically (1A) or macroscopically (1B)
  2. Upper 2/3 vagina (2A) or parametrium (2B)
  3. Lower 1/3 vagina (3A) or pelvic sidewall/hydronephrosis/non-functioning kidney (3B)
  4. Mucosa of bladder/rectum (4A) or distant sites (4B)
72
Q

Spread of cervical carcinoma

A

Local

Lymphatic - iliac nodes, retrograde to lower vagina

Haematogenous - uncommon. Vaginal plexus to portal circulation

73
Q

Causes of death in cervical carcinoma

A 
Renal failure
Haemorrhage
Super-added infection
Blood-borne metastasis
Iatrogenic (PE post surgery)
74
Q

What constitutes an adequate pap smear?

A

Endocervical cells show TZ has been sampled

Cells not obscured by blood/exudate/drying out

75
Q

Protocol for epithelial cell abnormalities on pap smear

A

ASC-US: repeat after 1 year. Colposcopy if 3x consecutive

LSIL: repeat smear after 1 year. Colp if LSIL x2

HSIL: immediate colposcopy

Squamous carcinoma: immediate colposcopy

76
Q

Pap smear report includes…

A
  1. Adequacy of smear
  2. Epithelial or glandular cell abnormalities
  3. Organisms
77
Q

Treatment based on cervical biopsy

A

CIN1: follow up at colp clinic. Consider LLETZif persistent

CIN2-3: LLETZ. Cone biopsy/hyterectomy if margins involved

Stage 1A1 and no lymphovascular invasion: cone biopsy

1A2: total abdominal hysterectomy and PL

1B1: radical hysterectomy and PL

Higher stages: chemoradiation + brachytherapy

Post op chemoradiation if lymph nodes prove positive

78
Q

SA pap smear policy

A

3 smears in lifetime
Begin at the age of 30
Repeated 10 yearly

79
Q

Endometeial carcinoma type 1

A

Unopposed oestrogen (PCOS, HRT, obesity)
Hyperplasia pathway
Tendency for contiguous spread
Good prognosis with surgery

80
Q

Endometrial carcinoma type 2

A 
Older, atrophic epithelium
Serous pathway, p53 mutation
Tendency to disseminate in the pelvis
Needs chemotherapy
Bad prognosis
81
Q

Types of gestational trophoblastic disease

A
  1. Hydatidiform mole: partial, complete or invasive

2. Choriocarcinoma

82
Q

Hydatidiform mole

A

Fertilisation of one ovum by 2 spermatozoa

Molar tissue with grape-like clusters of chorionic villi and varying degrees of trophoblastic proliferation

83
Q

Partial mole

A

Usually triploid
Molar tissue with moderate trophoblastic proliferation
Often stillborn fetus or fetal parts
Little malignant potential

84
Q

Complete/classical mole

A

46XX, totally paternal origin
Molar tissue without normal villi/fetal parts
Marked trophoblastic proliferation and malignant potential

85
Q

Invasive mole

A

Variant of complete mole with extension to the parametrium

May metastasize haematogenously

86
Q

Choriocarcinoma

A

Highly malignant with propensity for haemotogenous spread
Syncytio/cytotrophoblastic origin
Follows hydatidiform mole or normal/aborted pregnancy
Good response to chemotherapy

87
Q

Ligamentous supports of the uterus

A 
Pubovesical
Transverse cervical
Uterosacral
Round ligament
Broad ligament
88
Q

Chem path perimenopause

A

FSH rises 1-2 years before menopause

LH initially unchanged

89
Q

Chem path post menopause

A

FSH and LH rise significantly. FSH > LH

>90% decrease in oestrogen

3rd Year (7 decks)

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