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Case 13 Flashcards

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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
Phases of the uterine cycle
Menstrual Proliferative Secretory Ischaemic
25
Histological appearance of primordial follicles
Squamous, flattened granulosa cells
26
Histological appearance of primary follicles
Cuboidal granulosa cells, unilayer | Zona pellucida begins to form
27
Histological appearance of early secondary follicles
Stratified cuboidal granulosa cells Zona pellucida fully assembled Theca differentiating
28
Histological appearance of pre antral secondary follicle
Well differentiated theca | Beginnings of antrum are seen as liquor-filled spaces between granulosa cells
29
Histological appearance of tertiary/antral/Graafian follicle
Antrum Cumulus oophorus Corona radiata
30
Follicular events following ovulation
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
31
Histological appearance of atretic follicles
Thick, folded basement membrane Delaminating granulosa cells Invading macrophages
32
Development of the corpus luteum
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
33
Characteristics of steroid secreting cells
Lipid droplets Well developed smooth ER Mitochondria with tubular cristae
34
Histological appearance of the corpus albicans
Fibrous ovarian stroma with blood vessels
35
Theca interna cell functioning
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
36
Granulosa lutein cell functioning
Under the control of both LH and FSH Store cholesterol for progesterone synthesis Convert androstenedione to estradiol
37
Granulosa cell functioning
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
When do GCs acquire LH receptors?
Graafian follicle stage
39
What maintains the oocyte in arrested prophase 1?
Oocyte maturation inhibiting factor
40
When is the first polar body formed and where is it found?
Following completion of meiosis 1 just before ovulation. Found in the perivitilline space
41
What type of molecule makes up the zona pellucida?
Glycoproteins
42
Effects of the LH surge on the Graafian follicle
Halts oestrogen production Initiates second meiotic division Local prostaglandin production causes vascular follicular swelling and proteolytic enzyme activity After ovulation,causes luteinisation
43
Histology: uterine proliferative phase
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
Histology: uterine secretory phase
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
Histology: endocervix
Large branched tubular glands Columnar mucous secreting epithelium with some cilia Fibroelastic stroma
46
Histology: ectocervix
Stratified squamous epithelium
47
Potential risks: cervical transformation zone
Early puberty - infections Nabothian cysts Dysplasia Carcinoma
48
Pap cytology
Acidophilic cells: fully differentiated, from superficial layer, pyknotic nuclei. Abundant at ovulation Basophilic cells: from deeper layers, plumper normal-looking nuclei. Abundant postovulatory
49
Anatomic regions of the uterine tube
Infundibulum Ampulla Isthmus Intramural
50
Uterine tube histology
Epithelium: columnar cells - cilliated cells and non-cilliated peg cells with apical microvilli Lamina propria Muscle layer: inner circular outer longitudinal Mesothelial serosa
51
Characteristic sign of HPV on pap smear
Koilocytosis
52
Structure of the vagina
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
Where are Skene's glands found?
Adjacent to the urethral meatus
54
What constitutes an unnatural death?
Application of force, physical, chemical or other factors Act of omission or comission Procedure-related death Unexpected/unexplained death
55
Pathogenesis of TB in the female genital tract
Haematogenous spread to the uterine tubes Chronic inflammation with granulomas and caseous necrosis Direct spread to the uterus causes tuberculous endometritis
56
Commonest site of extrauterine pregnancy
Uterine tube
57
Causes of tubal ectopic pregnancy
Partial obstruction following salpingitis | Delayed pickup of the ovum by the fimbriae
58
Major complication of a tubal ectopic
Rupture and haemorrhage due to trophoblastic invasion of the wall of the uterine tube
59
Ectopic endometrial tissue may arise due to...
``` Retrograde spread during menstruation Implantation during c/s Metaplasia Lymphatic spread involving nodes Blood spread ```
60
Endometriosis sites
``` Ovary, tubes, pouch of Douglas GIT (recto-sigmoid) Umbilicus and surgical scars Pelvic lymph nodes Distant sites - lungs ```
61
Macroscopic appearance endometeiosis
"Chocolate cysts" with fibrosis due to cyclical haemorrhage
62
Microscopic appearance endometriosis
Endometrial glands plus steoma | Haemosiderin-laden macrophages
63
Complications of endometriosis
Infertility Adhesions Intermittent intestinal obstruction Endometrioid carcinoma
64
Cervical CA epidemiology
Commonest non-cutaneous malignancy in SA Age 20-80 (commonest 35-50) Regarded as STD
65
Risk factors for cervical cancer
``` High risk HPV infection Promiscuity, early debut, parity, STIs Cigarette smoking Oral contraceptive Long interval since last pap smear Low SES ```
66
Cervical biopsy grading
CIN 1, 2 and 3 (British system)
67
Cervical cytology grading
LSIL/HSIL (Bethesda system)
68
Macroscopic appearance of cervical carcinoma
Ulcerating, exophytic or nodular
69
Microscopic appearance of cervical carcinoma
Squamous carcinoma with or without keratin
70
Adenocarcinoma
Much less common Some related to HPV Age 30-60
71
Staging cervical carcinoma
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
Spread of cervical carcinoma
Local Lymphatic - iliac nodes, retrograde to lower vagina Haematogenous - uncommon. Vaginal plexus to portal circulation
73
Causes of death in cervical carcinoma
``` Renal failure Haemorrhage Super-added infection Blood-borne metastasis Iatrogenic (PE post surgery) ```
74
What constitutes an adequate pap smear?
Endocervical cells show TZ has been sampled | Cells not obscured by blood/exudate/drying out
75
Protocol for epithelial cell abnormalities on pap smear
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
Pap smear report includes...
1. Adequacy of smear 2. Epithelial or glandular cell abnormalities 3. Organisms
77
Treatment based on cervical biopsy
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
SA pap smear policy
3 smears in lifetime Begin at the age of 30 Repeated 10 yearly
79
Endometeial carcinoma type 1
Unopposed oestrogen (PCOS, HRT, obesity) Hyperplasia pathway Tendency for contiguous spread Good prognosis with surgery
80
Endometrial carcinoma type 2
``` Older, atrophic epithelium Serous pathway, p53 mutation Tendency to disseminate in the pelvis Needs chemotherapy Bad prognosis ```
81
Types of gestational trophoblastic disease
1. Hydatidiform mole: partial, complete or invasive | 2. Choriocarcinoma
82
Hydatidiform mole
Fertilisation of one ovum by 2 spermatozoa | Molar tissue with grape-like clusters of chorionic villi and varying degrees of trophoblastic proliferation
83
Partial mole
Usually triploid Molar tissue with moderate trophoblastic proliferation Often stillborn fetus or fetal parts Little malignant potential
84
Complete/classical mole
46XX, totally paternal origin Molar tissue without normal villi/fetal parts Marked trophoblastic proliferation and malignant potential
85
Invasive mole
Variant of complete mole with extension to the parametrium | May metastasize haematogenously
86
Choriocarcinoma
Highly malignant with propensity for haemotogenous spread Syncytio/cytotrophoblastic origin Follows hydatidiform mole or normal/aborted pregnancy Good response to chemotherapy
87
Ligamentous supports of the uterus
``` Pubovesical Transverse cervical Uterosacral Round ligament Broad ligament ```
88
Chem path perimenopause
FSH rises 1-2 years before menopause | LH initially unchanged
89
Chem path post menopause
FSH and LH rise significantly. FSH > LH | >90% decrease in oestrogen

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