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Pathology Flashcards

1
Q

what are the ovarian stages of the menstrual cycle

A

follicular (development of follicles)
ovulation
luteal phase (development of corpus luteum, end in pregnancy/ start of period)

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2
Q

what are the uterine phases of the menstrual cycle

A

menstrual phase
proliferative phase
secretory phase

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3
Q

how long does the proliferative (uterine) phase of menstruation usually last

A

14 days- is same in most women

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4
Q

what happens to the endometrium in the different uterine phases of menstruation - which hormones are in control in each phase

A

proliferative- grows, oestrogen

secretory- builds secretions, progesterone

menstrual- necrosis, sheds, withdrawal of progesterone

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5
Q

what happens to the endometrium after fertilisation- what hormones are in control

A

hypersecretion, decidualisation

progesterone and HCG

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6
Q

at what days in the cycle do the different uterine phases of menstruation happen

A

proliferative- D1-12
secretory- D16-28
menstrual D1-3

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7
Q

what happens to the endometrium post menopause

A

is inactive/ atrophic

non cycling

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8
Q

what secretes the porgesterone needed in the secretory phase

A

corpus luteum

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9
Q

what is a graafia follicle

A

mature vesicular follicles= ooctye + granulosa cells

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10
Q

what is seen histologically in the proliferative stage

A

glandular epithelium

glands are very circular

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11
Q

what is the corpus albicans

A

what happens when the corpus luteum degenerates

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12
Q

what is seen histologically in the secretory phase

A

increasing tortuosity of glands

lumenal secretions

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13
Q

what are the indications for endometrial sampling (biopsy)

A

abnormal uterine bleeding
investigation for infertility
spontaneous and therapeutic abortion (looking for molar pregnancy)
assessment of response to hormonal therapy
endometrial ablation
work up prior to hysterectomy for benign indications
incidental finding of thickened endometrium on scan
endometrial cancer screening in high risk patients

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14
Q

what increases your risk of endometrial cancer

A

obesity

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15
Q

what is menorrhagia

A

prolonged and increased menstrual flow

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16
Q

what is metrorrhagia

A

regular intermenstrual bleeding

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17
Q

what is polymenorrhoea

A

menses occurring at <21 day interval

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18
Q

what is polymenorrhagia

A

increased bleeding and frequent cycle

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19
Q

what is menometrorrhagia

A

prolonged menses and intermenstrual bleeding

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20
Q

what is amenorrhagia

A

absence of menstruation > 6 months

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21
Q

what is oligomenorrhoea

A

menses at intervals of > 35 days

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22
Q

what does DUB stand for

A

dysfunctional uterine bleeding

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23
Q

what is post menstrual bleeding

A

abnormal uterine bleeding after > 1 year of no bleeding

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24
Q

what can cause AUB in adolescence/ early reproductive life

A

usually caused by anovulatory cycles (ovum not released)
pregnancy/ miscarriage
endometritis
bleeding disorders

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25
Q

what is endomitritis

A

inflammation of the uterus lining, usually due to infection

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26
Q

what can cause AUB during reproductive age/ perimenopause

A

pregnancy/ miscarriage
DUB (anovulatory cycles, luteal phase defects)
endomitritis
endometrial/ endocervical polyp
leiomyoma (smooth muscle tumour- aka fibroid)
adenomyosis (endometrial tissues (glands and stroma) within the myometrium (muscle of uterus))
exogenous hormone effects
bleeding disorders
hyperplasia
neoplasia- cervical, endometrial

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27
Q

what are the causes of AUB post menopause

A

atrophy (will cause tiny amount on bleeding, only once)
endometrial polyp
exogenous hormones (HRT- causes some proliferation of endometrium, tamoxifen (taken in breast cancer, has proestrogenic effect))
endometritis
bleeding disorders

hyperplasia
endometrial carcinoma
sarcoma

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28
Q

what are the methods of assessing the endometrium

A

transvaginal US- endometrial thickness of >4mm in postmenopausal women (16mm in premenopausal) is indication for a biopsy

hysteroscopy

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29
Q

what are the methods of sampling the endometrium

A

endometrial pipelle (no dilatation/ anaesthesia, outpatient, safe but limited sample)

dilatation and curretage (most thorough sampling methods, can miss 5% hyperplasia/ cancers)

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30
Q

what history details are required on a endometrial sample

A 
age
date of LMP and length of cycle 
patterns of bleeding 
hormones
recent pregnancy
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31
Q

when in menstrual cycle do you not want to take an endometrial cycle

A

in menstrual phase (as least informative sample)

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32
Q

what is dysfunctional uterine bleeding

A

irregular bleeding that reflects a disruption in the normal cyclic pattern of ovulatory hormonal stimulation to the endometrial linging
(= AUB but with no organic cause, is cause by hormone problem)

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33
Q

what causes the majority of dysfunctional uterine bleeding

A

anovulatory cycles

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34
Q

what are anovulatory cycles

A

when corpus luteum does not form
get continued disordered proliferation of functionalis layer of endometrium as a result as no progesterone

happens mostly in either end of reproductive age, due to e.g. PCOS, hypothalamic dysfunction, thyroid disorders, hyperprolactinaemia

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35
Q

what is luteal phase deficiency

A

insufficient progesterone or poor response by the endometrium to progesterone
causes abnormal follicular development (inadequate FSH/LH) = poor corpus luteum

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36
Q

what is seen histologically in the ednometrium in an anovulatory cycle

A

disorder proliferation
glands and stroma continue to grow
grands become wiggly shape and are not filled with any secretions

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37
Q

what are the organic causes of abnormal uterine bleeding

A

endometrium: endometritis, polyps, miscarriage
myometrium: adenomyosis, leiomyoma

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38
Q

what protects the endometrium from infection

A

cervical mucous plug

cyclical shedding

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39
Q

how is endometritis diagnosed histologically

A

abnormal pattern of inflammatory cells

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40
Q

what organisms commonly cause endometritis

A 
neisseria 
chlamydia 
TB
CMV
actinomyces (fungal organisms associated with intrauterine contraceptive device)
HSV
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41
Q

what are the causes of inflammation in endometritis without specific causative organisms

A 
IUC device 
postpartum 
postaboral 
post curettage 
chronic endometritis 
granulomatous (sarcoidosis, foreign body post ablation) 
associated with leiomyomata or polyps
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42
Q

what is associated with plasmacytic endometritis

A

pelvic inflammatory disease:

  • neiserria gonorrhoea
  • chlamydia
  • enteric organisms

will see plasma cell on histology

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43
Q

what do you get granulomatous endometritis is

A

TB, sarcoidosis

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44
Q

what are granulomas

A

balls of epithelial macrophages

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45
Q

what is the presentation of endometrial polyps

A

common
usually asymptomatic but may present with bleeding or discharge
often occur around and after the menopause
almost always benign
can tort or become ulcerated

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46
Q

what cancer can present as an endometrial polyp

A

endometrial carcinoma

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47
Q

what do you want to exlcude after miscarriage

A

a molar pregnancy

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48
Q

what is seen histologically of a miscarriage

A

chorionic villi - subunits of early placenta (these will have the DNA of the foetus)
can also have products of conception (foetal tissue, foetal RBCs)

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49
Q

what is a molar pregnancy

A

an abnormal form of pregnancy in which a non viable fertilised egg implants in the uterus (or fallopian tube)
a form of gestational trophoblastic disease which grows as a mass (characterised by swollen villi)

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50
Q

what are the types of molar pregnancy

A

complete- when one or two sperm combine with a egg that has lost its DNA, sperm then replicates to form a 46 chromosome set, only parental DNA is present

partial- when egg is fertilised by two sperm/ one sperm that reduplicates itself yielding the genotypes 69XXY (triploid), has both maternal and paternal DNA

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51
Q

which type of molar pregnancy is highest risk

A

complete hydatidiform moles have a higher risk of developing into choricarcinoma (a malignant tumour of trophoblast) which can grow and spread outwith the uterus

partial has low risk of complications

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52
Q

what is seen histologically in a molar pregnancy

A

abnormally proliferating trophoblast

chorionic villus

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53
Q

what does hydatid form mean

A

swollen

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54
Q

what is adenomyosis

A

when there are endometrial glands and stroma within the myometrium

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55
Q

what does adenomyosis cause

A

menorrhagia/ dysmenorrhoea

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56
Q

what is a leiomyoma

A

benign tumour of smooth muscle

found in locations other than uterus

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57
Q

what can leiomyomas present with

A

menorrhagia
infertility
mass effect
pain

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58
Q

what are the pathological features of a leiomyoma

A

can be single or multiple
mas distort uterine cavity
growth is oestrogen dependent
microscopically can see interlacing smooth muscle (spindle) cells

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59
Q

what is a leiomyosarcoma

A

malignant leiomyoma (rare)

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60
Q

what cells line the ectocervix (vaginal portion)

A

squamous epithelium
not keratinised
continuous with vaginal epithelium

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61
Q

what cells line the endocervix

A

glandular columnar epithelium

single layer of mucinous epithelium

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62
Q

what is the transformation zone

A

Squamo-columnar junction between ectocervical (squamous) and endocervical (columnar) epithelia

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63
Q

what happens to the position of the transformation zone throughout life

A

starts further out, moves towards cervix during menache as hormones make vagina more acidic = cervical erosion= physiological squamous metaplasia

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64
Q

what are nabothian follicles

A

dilated endocervical glands that form colloid structure when they dilate, benign

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65
Q

what is metaplasia

A

when one mature epithelium changes into another type of a mature epithelium

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66
Q

what are the features of cervicitis

A

often asymptomatic

can lead to infertility due to simultaneous fallopian tube damage

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67
Q

what can cause cervicitis

A
  • non specific acute/ chornic inflammation
  • follicular cervicitis- sub epithelial reactive lymphoid follicles present in cervix
  • chlamydia trachomatis- sexually transmitted
  • HSV infection
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68
Q

what are the features of a cervical polyp

A

localised inflammatory outgrowth
cause bleeding if ulcerated
not premalignant
usually always benign

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69
Q

what are the types of cervical carcinoma

A

squamous carcinoma

adenocarcinoma

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70
Q

what is CIN

A

cervical intraepithelial neoplasia- precursor lesion of cervical cancer, dysplasia of squamous cells
(pre invasive stage of cervical cancer)

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71
Q

how does HPV cause cancer

A

will infect basal cells
virus replicates within epithelial cells
intraepithelial hyperplasia
invasive cancer - virus integrated into host DNA

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72
Q

what are the high risk types of HPV

A

16,18

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73
Q

what are the risk factors for CIN/ cervical cancer

A

HPV infection (increased risk with increase no of sexual partners)
vulnerability of SC junction in early reproductive age (young age at first intercourse, long term use of oral contraceptives, non barrier contraception)
smoking
immunosuppression

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74
Q

what are the low risk types of HPV

A

6 and 11

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75
Q

what is the pathology of genital warts

A

HPV types 6 and 11
condyloma acuminatum:
-thicken papillomatous squamous epithelium with cytoplasmic vacuolation (koilocytosis)

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76
Q

what types of HPV cause genital warts

A

6 and 11

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77
Q

what is the pathology of cervical intraepithelial neoplasia due to HPV infection

A

types 16 and 18
infection epithelium remains flat
may show koilocytosis

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78
Q

what is koilocytosis

A

changes in epithelial cells due to HPV infection

normal -> koilocytosis -> CIN 1 -> CIN 2 -> CIN3

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79
Q

what happens to host DNA in invasive squamous carcinoma

A

HPV dna intergrated into host dna

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80
Q

when does cancer become cancer

A

when breaks away from/ through basal membrane

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81
Q

how long till HPV infection becomes high grade CIN and invasive cancer

A

high grade CIN= 6 months to 3 years

invasive cancer 5-20 years

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82
Q

what in the life process of HPV increases the risk of disease

A

persistence of the disease

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83
Q

what is the prevalence of HPV

A

15-25years 30-50%
25-35years 10-20%
>35years 5-15%

80% cumulative prevalence in a lifetime

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84
Q

what is dyskaryosis

A

abnormal cytologic changes of squamous epithelial cells characterized by hyperchromatic nuclei and/or irregular nuclear chromatin
seen in HPV

85
Q

what changes happen to cells in HPV infection

A

big nucleus in relation to cytoplasm

86
Q

where does CIN affect

A

transformation zone

can involve large area

87
Q

how is CIN discorvered

A

asymptomatic
not visible to naked eye
detected by cervical smear

88
Q

What are the histological features of CIN

A 
Delay in maturation/differentiation:   
-immature basal cells occupying more of epithelium
Nuclear abnormalities:
-hyperchromasia
-increased nucleocytoplasmic ratio
-pleomorphism 
Excess mitotic activity
-situated above basal layers
-abnormal mitotic forms

Often koilocytosis (indicating HPV infection) also present

89
Q

where should mitotic activity happen

A

on in basal layer

90
Q

how is CIN graded

A

1-3 depending on histological factors

91
Q

what are the features of CIN 1

A

Basal 1/3 of epithelium occupied by abnormal cells.
Raised numbers of mitotic figures in lower 1/3.
Surface cells quite mature, but nuclei slightly abnormal

92
Q

what are the features of CIN 2

A

Abnormal cells extend to middle 1/3.
Mitoses in middle 1/3
Abnormal mitotic figures

93
Q

what are the features of CIN 3

A

Abnormal cells occupy full thickness of epithelium.

Mitoses, often abnormal, in upper 1/3.

94
Q

when does dysplasia become cancer

A

when abnormal cells goes through basement membrane (stromal invasion)

95
Q

what is the most common type of malignant cervical cancer

A

invasive squamous carcinoma

96
Q

what does invasive squamous carcinoma develop form

A

CIN

preventable bu screening

97
Q

what type of lesion is CIN

A

squamous

98
Q

how common and severe is cervical cancer

A

2nd most common worldwide, 12th in scotland

70.1% 5 year survival

99
Q

what are the stages of invasive squamous carcinoma

A

Stage 1A1 - depth up to 3mm, width up to 7mm
Stage 1A2 - depth up to 5mm, width up to 7mm
Low risk of lymph node metastases
Stage 1B - confined to the cervix
Stage 2 - spread to adjacent organs (vagina, uterus, etc..)
Stage 3 - involvement of pelvic wall
Stage 4 - distant metastases or involvement of rectum or bladder.

100
Q

what does the treatment of invasive squamous carcinoma depend on

A

if spread outwith cervix- chemo + radio

if not then radical hysterectomy

101
Q

what are the symptoms of invasive squamous cervical carcinoma

A 
Usually none at microinvasive and early invasive stages  (detected at screening)
Abnormal bleeding:
-Post coital
-Post menopausal
-Brownish or blood stained vaginal discharge
-Contact bleeding – friable epithelium
Pelvic pain
Haematuria / urinary infections
Ureteric obstruction / renal failure
102
Q

how does squamous carcinoma spread

A

Local -> uterine body, vagina bladder, ureters, rectum
Lymphatic (early) -> pelvic, para-aortic nodes
Haematogenous (late) -> liver, lungs, bone

103
Q

is squamous carcinoma or adenocarcinoma in cervix more common

A

squamous more common

104
Q

what is CGIN

A

cervical glandular intraepithelial neoplasia - preinvasive phase of endocervical adenocarcinoma

105
Q

what cells does CGIN originate from

A 
endocervical epithelium
(some are mixed)
106
Q

why is CGIN harder to diagnose that CIN

A

more difficult to diagnose on a smear

screening less effective

107
Q

what causes CGIN

A

HPV

108
Q

what is CGIN sometimes associated with

A

CIN

109
Q

what are the histological features of CGIN

A

Glands colonized by CGIN

Big nuclei, mitotic figures

110
Q

does cervical squamous or adenocarcinoma have worst prognosis

A

endocervical adenocarcinoma has poorer prognosis

111
Q

what is the epidemiology of cervical adenocarcinoma

A

Higher S.E. (socioeconomic) Class than CIN
Later onset of sexual activity
Smoking
HPV again incriminated, particularly HPV18.

112
Q

what is VIN, VaIN, AIN

A

Vulvar Intraepithelial Neoplasia, VIN (aka pagets disease)
Vaginal Intraepithelial Neoplasia, VaIN
Anal Intraepithelial Neoplasia, AIN

113
Q

what are the features of vulvar intraepithelial disease

A

variable behaviour- less predictable than CIN
Young women: often multifocal, recurrent or persistent causing treatment problems.
Older women: greater risk of progression to invasive squamous carcinoma.
often HPV related (non HPV related associated with lichen sclerosis/ planus - inflammatory conditions)
often also have CIN and VaIN

114
Q

what are the features of vulvar invasive squamous carcinoma

A

Usually elderly women, ulcer or exophytic mass.
Can arise from normal epithelium or VIN.
Mostly well differentiated (verrucous are an extremely well differentiated type).

115
Q

what is the most important prognostic factor for vulvar invasive squamous carcinoma

A

spread to inguinal lymph nodes
90% 5 year survival – node negative
<60% 5 year survival – node positive

116
Q

what is the treatment for vulvar invasive squamous carcinoma

A

Surgical treatment – radical vulvectomy and inguinal lymphadenectomy.

117
Q

what are the features of vulvar pagets disease

A

Crusting rash.
Tumour cells in epidermis, contain mucin.
Mostly no underlying cancer, tumour arises from sweat gland in skin (intrapeothelial)
can have underlying cancer
Spreads along the vulva and ometimes to anus, vaginal, thighs
Painful, itchy, weeping, oozing

118
Q

what infection affect the vulva

A

Candida (Particularly diabetics)
Vulvar warts (HPV 6 & 11)
Bartholin’s gland abscess (blockage of gland duct)

119
Q

are are non neoplastic vulval disorders

A 
(inflammatory diseases)
Lichen Sclerosis
Other dermatoses
Lichen planus
Psoriasis
120
Q

when do women get vulva atrophy

A

post menopausal

121
Q

what do women with Vaginal intraepithelial neoplasia often have

A

cervical and vulval lesions

122
Q

who gets vaginal squamous carcinoma

A

elderly women

Less common than cervical and vulval counterparts

123
Q

can you get vaginal melanoma

A

yes

124
Q

are primary cancers of the vagina common

A

Cancer of vagina has usually spread from somewhere near by

Primary cancers of vagina rare- but if it is will be squamous or melanoma

125
Q

Pale nodules separate from each other, circular, whirled surface, round and well circumscribed, no areas of necrosis/ haemorrhage, in uterus= ?

A

leiomyoma (fibroid, benign tumour of smooth muscle)

126
Q

when does a cancer become microinvasive

A

when it breaks through the BM

127
Q

where do carcinomas almost always spread first

A

lymphatics

128
Q

what are the symptoms of ovarian cancer

A

vague- abdo discomfort, bloating

129
Q

are ovarian and testicular teratomas benign or malignant

A

ovarian almost always benign

testes almost always malignant

130
Q

Endometrial glands and stroma outside the wall of the uterus= ?

A

endometriosis

131
Q

what do complete molar pregnancies carry the risk of

A

choriocarcinoma

132
Q

what are the causes of dysfunctional uterine bleeding

A 
endometrial polyps 
endometrial hyperplasia (simple, complex or atypical - precursor of carcinoma)
133
Q

are endometrial polyps common

A

yes

often occur around/ after the menopause

134
Q

are endometrial polyps usually benign or malignant

A

typically benign, can be malignant

135
Q

what causes endometrial hyperplasia

A

often unknown

can be persistent oestrogen stimulation

136
Q

how does endometrial hyperplasia present

A

abnormal bleeding (dysfunctional uterine or postmenopausal)

137
Q

what are the differences between simple, complex and atypical endometrial hyperplasia

A

simple- general distrubtion of stroma and (dilated but not crowded) glands, normal cytology

complex= focal distribution of crowded glands with normal cytology

atypical= focal distribution of crowded glands with atypical cytology (nuclei enlarged and no longer line along bases of cells, change in colour)

138
Q

what is the management of atypical endometrial hyperplasia with no other risk factors

A

hysterectomy (high risk of progression to cancer)

139
Q

what happens to endometrial glands in hyperplasia

A

become bigger, less circular, cystically dilated

loose stroma between glands

140
Q

what hystological sign means endometrial hyperplasia has become cancer

A

when glands start to fuse

141
Q

who gets endometrial cancer

A

Peak incidence 50 ‐ 60 years; uncommon under 40

In young women, consider underlying predisposition e.g. polycystic ovary syndrome or Lynch syndrome (HNPPC)

142
Q

what cancers does lynch syndrome increase the risk of

A

colorectal
endometrial
ovarian

143
Q

what are the two main types of endometrial cancer

A 
endometriod carcinoma (most common)
serous carcinoma
144
Q

how does endometrial cancer generally present

A

abnormal bleeding (typically post menopausal)

145
Q

what is the precursor lesion for endometrioid carcinoma

A

atypical hyperplasia

usually due to high levels of oestrogen stimulating the endometrium (obesity)

146
Q

what is the precursor lesion for serous endometrial carcinoma

A

serous intraepithelial carcinoma = atrophic endometrium- occurs in older women

147
Q

what does an endometrial carcinoma look like macroscopically

A

large uterus that is polypoid

148
Q

what are the majority of endometrial carcinomas

A

well differentiated (grade 1) adenocarcinoma (endometrioid)

149
Q

how do endometrial carcinomas spread

A

directly into myometrium and cervix
lymphatics
haematogenous

150
Q

what biopsy for suspected endometrial carcinoma

A

pipelle

151
Q

Tx for endometrial carcinoma

A

depends on grade: 1= surgery , 2-3= scan to see if spread, don’t want to remove uterus when tumour has already spread - chemo and radio

152
Q

which type of endometrial carcinoma is more likely to spread

A

serous

153
Q

what are the features of endometrioid and mucinous carcinomas

A

adenocarcinomas
80% of endometrial cancer
related to unopposed oestrogen
associated with atypical hyperplasia precursor lesion
PTEN, KRAS, PIK3CA mutations
microsatellite instability (short strands of DNA within cells, lynch syndrome)

154
Q

what are the features of serous and clear cell endometrial carcinomas

A

not associated with unopposed oestrogen
affects elderly post menopausal women
TP53 often mutated and overexpressed (makes it more aggressive)
serous and clear cell phenotypes
precursor lesion serous endometrial intrapepithelial carcinoma
more aggressive than endometrioid/ mucinous carcinoma- surgery more extensive and adjuvant chemo/radio often used

155
Q

why is obesity a risk factor for endometrial cancer

A

the endocrine and inflammatory effects of adipose tissue:

Adipocytes express aromatase that converts ovarian androgens into oestrogens, which induce endometrial proliferation.

Sex hormone-binding globulin levels are lower in obese women, and therefore the level of unbound, biologically active hormone is higher.

Insulin action is often altered in obese women: The level of insulin-binding globulins is reduced and free insulin levels are elevated. Insulin/insulin-like growth factors (IGF) exert proliferative effect on endometrium.

156
Q

how can you reduce the risk of obesity and endometrial cancer

A

lose weight lol

157
Q

what is lynch syndrome

A

hereditary non polyposis colorectal cancer
cancer predisposition syndrome (colorectal, ovarian and endometrial)
defective DNA mismatch repair gene
AD inheritance

158
Q

how can tumour due to lynch syndrome be identified

A

Immunohistochemistry staining of the tumour for mismatch repair proteins
Lynch syndrome tumours also show microsatellite instability (MSI), a characteristic of defective mismatchrepair

159
Q

how do serous/ clear cell carcinomas (endometrial) spread

A

along fallopian tube mucosa and peritoneal surfaces

can present with extrauterine disease

160
Q

what are the characteristics histologically of serous carincoma

A

complex papillary and/or glandular architecture with diffuse, marked nuclear pleomorphism

161
Q

why does endometrioid carcinoma usually have a good prognosis

A

as usually confined to

uterus at presentation

162
Q

what does the prognosis of endometrial carcinoma depend on

A

Stage
Histological grade
Depth of myometrial invasion

163
Q

what are the treatment options for endometrial carcinoma

A

hysterectomy

chemo/ radio

164
Q

how are endometrial cancers graded

A

Endometrioid carcinoma are primarily graded by their architecture (how well differentiated they are)

Grade 1 5% or less solid growth
Grade 2 6-50% solid growth
Grade 3 >50% solid growth

Serous carcinoma and clear cell carcinoma are not formally graded

165
Q

what are the stages of endometrial cancer

A

Stage I Tumour confined to the uterus

IA no or < 50% myometrial invasion
IB Invasion equal to or > 50% of myometrium

II Tumour invades cervical stroma

III Local and or regional tumour spread
IIIA Tumour invades serosa of uterus and/or adnexae
IIIB Vaginal and/or parametrial involvement
IIIC Metastases to pelvic and/or para-aortic lymph nodes

IV Tumour invades bladder and or bowel mucosa (IVA) and/or distant metastases (IVB)

166
Q

where are the lymphatic and vessels of the myometrium

A

outer half

167
Q

what are the less common endometrial tumours

A

Endometrial stromal sarcoma (Tumour arising from endometrial stroma)

Carcinosarcoma- (produces mesenchyma tissue- forms malignant cartilage, bone and neural tissue
Mixed tumour with malignant epithelial and stromal elements)

168
Q

what are the features of endometrial stromal sarcoma

A

Rare, cells resemble endometrial stroma.
histologically looks like stroma separating the myometrium- destructive growth
Infiltrate myometrium and often lymphovascular spaces
Typically presents with abnormal uterine bleeding but initial presentation may be as metastasis (most commonly ovary or lung)

169
Q

what is usually the outcome of a endometrial carcinosarcoma

A

usually poor

worse is phabdomyosarcomatous component present

170
Q

what are the macroscopic characteristics of a carcinosarcoma

A

Large bulky tumour filling cavity, commonly protrudes through the cervical canal.

171
Q

what are the smooth muscle tumours of the myometrium

A

Leiomyoma (fibroid)- very common

Leiomyosarcoma (rare)

172
Q

what are leiomyomas associated with

A

menorrhagia

infertility

173
Q

what is a leiomyosarcoma

A

A malignant smooth muscle tumour commonly displaying a spindle cell morphology
The most common uterine sarcoma

174
Q

how do leiomyosarcomas present

A

Most occur in women >50 years

abnormal vaginal bleeding, palpable pelvic mass and pelvic pain

175
Q

what is the prognosis of leiomyosarcoma

A

Poor prognosis even if confined to uterus at time of diagnosis
Overall 5 year survival rates 15-25%, stage is most powerful prognostic factor

176
Q

what are the types of ovarian cyst

A

(can arise from any element of the ovary)

  • follicular (PCOS)
  • luteal (corpus luteum)
  • endometriotic
  • epithelial
  • mesothelial
177
Q

what are the features of a follicular ovarian cyst

A

very common
can form when ovulation doesnt occur (PCOS)- follicle doesnt rupture, grows until it becomes a cyst
thin walled lined by granulosa cells
usually resolve after a few months

178
Q

what is endometriosis

A

endometrial glands and stroma outside the uterine body

179
Q

what can endometriosis cause

A

pelvic inflammation
infertility (scarring and adhesions can affect petency of fallopain tube, compression of ovary can cause loss of normal parenchyma)
pain

180
Q

what are the possible sites of endometriosis

A 
ovary (chocolate cysts) 
pouch of douglas 
peritoneal surfaces (inc uterus) 
cervix 
vulva 
vagina 
bladder 
bowel
181
Q

what is endometrioma

A

ovarian endometriosis

endometrial tissue on the ovary

182
Q

what causes ovarian endometriosis

A

regurgitation of tissue
metaplasia
vascular or lymphatic dissemination

183
Q

what is the macroscopic appearance of ovarian endometriosis

A

peritoneal spots or nodules
fibrous adhesions
chocolate cysts

184
Q

what is the microscopic appearance of ovarian endometriosis

A

endometrial glands and stroma

haemorrhage, inflammation, fibrosis

185
Q

what are the possible complications of endometriosis

A

pain
cyst formation
adhesions
infertility
ectopic pregnancy (caused by scarring and fusions of pilecae of tube- finger like processes in lumen)
malignancy (endometrioid carcinoma/ clear cell)

186
Q

what are the types of ovarian tumours

A 
epithelial- most common malignant (serous, mucinous, endometrioid, clear cell, brenner)
-germ cell (teratoma) 
-sex-cord/ stromal 
-metastatic 
others
187
Q

what are the types epithelial ovarian tumours

A 
serous 
mucinous 
endometrioid 
clear cell 
brenner 
undifferentiated carcinoma
188
Q

why do you get epithelial tumour of ovary when no epithelium in ovary (mesothelium covering stroma and eggs)

A

as when eggs break through mesothelium some cells get dragged back into ovary and under go metaplasia

189
Q

how are epithelial ovarian tumours subdivided

A

benign: No Cytological abnormalities, proliferative activity absent or scant, no stromal invasion
borderline: Cytological abnormalities, proliferative, no stromal invasion
malignant: stromal invasion

190
Q

how are serous ovarian carcinomas divided

A

into low or high grade as have different precursor lesion
-High grade serous carcinoma
Serous tubal intraepithelial carcinoma (STIC)
Most cases are essentially tubal in origin

-Low grade serous carcinoma
Serous borderline tumour

191
Q

what are endometrioid and clear cell ovarian cancer associated with

A

endometriosis of the ovary

lynch syndrome

192
Q

are endometrioid cancer usually good or bad

A

usually low grade and early stage

193
Q

how is the diagnosis of endometrioid cancer of ovary usually made

A

cytology of ascitic fluid

194
Q

what is a brenner tumour

A

tumour of ovary
transitional type epithelium
usually benign
borderline/ malignant variants rare

195
Q

what makes up a teratoma

A 
cystic, containing sebum and hair
ectoderm, mesoderm and endoderm
skin, respiratory epithelium, gut, fat common
can rarely become malignant
arises from germ cell in ovary
196
Q

what is a dermoid cyst

A

mature teratoma

197
Q

what is the most common germ cell tumour

A

mature teratoma

198
Q

what are the other types of teratoma

A 
Immature teratoma
Dysgerminoma (most common malignant, almoat always in children and young women)
Yolk sac tumour
Choriocarcinoma
Mixed germ cell tumour
199
Q

what are the ovarian sex chord/ stromal tumour

A

Fibroma/Thecoma
Benign
-May produce oestrogen causing uterine bleeding

Granulosa cell tumour

  • All are potentially malignant
  • May be associated with oestrogenic manifestations (thickened endometrium and bleeding)

Sertoli-Leydig cell tumours
-Rare, may produce androgens

200
Q

what cancers can metastasise to ovaries

A

stomach
colon
breast
pancreas

201
Q

what do mets to the ovaries look like

A

bilateral and small

202
Q

how is ovarian cancer staged

A

1A tumour limited to one ovaries

1B tumour limited to both ovaries

1C Cancer involving ovarian surface/
rupture/surgical spill/tumour in washings

2A Extension or implants on uterus/fallopian tube

2B Extension to other pelvic intraperitoneal

3A Retroperitoneal lymph node
Metastasis or microscopic extrapelvic peritoneal involvement

3B Macroscopic peritoneal metastasis beyond pelvis up to 2cm in dimension

3C Macroscopic peritoneal metastasis >2cm in dimension

4 Distant metastasis

203
Q

what is salpingitis

A

inflammation of the fallopian tube due to infection

204
Q

what cancer can you get in the fallopian tubes

A

Serous tubal intraepithelial carcinoma

205
Q

what is an ectopic pregnancy

A

Implantation of a conceptus outside the endometrial cavity

206
Q

where can ectopic pregnancies happen

A

Commonest site is Fallopian tube (often ruptures)

May occur in ovary, peritoneum, cervix, interstitial (myometrium)

207
Q

how might an ectopic pregnancy be fatal for women

A

fatal haemorrhage

208
Q

what is the presentation of an ectopic pregnancy

A

female of reproductive age with amenorrhoea and acute hypotension or an acute abdomen

Reproduction (51 decks)

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