cervix, vulva, vagina Flashcards

1
Q

normal ectocervixn- cell layers

A

exfoliating cells, superficial cells, intermediate cells, basement membrane

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2
Q

which part of the cervix can you feel in vaginal canal?

A

ectocervix

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3
Q

which part has hard squamous cells?

A

ectocervix

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4
Q

which part has soft columnar glandular cells?

A

endocervix

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5
Q

hard squamous becomes soft columnar glandular cells?

A

transition zone

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6
Q

the position of the tz alters throughout life. this is physiological. what is it a response to?

A

menarche, pregnancy, menopause

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7
Q

which part is the opening of the uterus?

A

endocervix

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8
Q

what is tz also known as?

A

squamo columnar junction

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9
Q

exposure of delicate endoecervical epithelium to acid environment of vagina leads to ?

A

physiological squamous metaplasia

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10
Q

what is a nathobian cyst

A

mucus filled cyst on the surface of the cervix. caused by squamous cells growing over columnar cells

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11
Q

what happenst to nathobian cysts?

A

usually disappear on their own

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12
Q

how can cervicitis lead to infertility?

A

can cause simultaneous silent fallopian tube damage

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13
Q

cervicitis can be? (4)

A

non specific, follicular, chlamydia, hsv infection

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14
Q

what kind of cells would you see in follicular cervicitis?

A

lymphoid follicles

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15
Q

cervical polyp - when can it cause bleeding? is it malignant?

A

it can cause bleeding but is not malignant

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16
Q

two main types of cervical cancer

A

squamous and aden squ ad

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17
Q

how does HPV infect the cervical cells

A

infects epithelial cells in the cervical mucosa. HPV DNA integrates into the cellular genome when causing cancer

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18
Q

within weeks you can get viral replication

A

90% heal within 2 years

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19
Q

over 10-30 years, how many will develop into an invasive cancer?

A

0.8%

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20
Q

why does having many sexual partners increase risk of cervical cancer?

A

increases likelihood and time exposed to high risk HPV

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21
Q

smoking increases risk of cervical cancer by?

A

3

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22
Q

age at first intercourse, long term use of oral contraceptive and non use of barrier contraception all increase risk of cervical cancer

A

immunosuppression also

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23
Q

in genital warts, koilocytosis is seen, how can this be picked up?

A

cervical smear

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24
Q

how long does it take to get from HPV infection to high grade CIN?

A

6 months - 3 years

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25
Q

high grade CIN - invasive cancer?

A

5-20 years

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26
Q

pre i invasive stage of cervical cancer, occurs at transformation zone, can involve large area, not visible to naked eye, asymptomatic, detectable by cervical screening

A

CIN

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27
Q

normal pathway of CIN?

A

normal epithelium - koilocytosis - CIN 1-2-3

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28
Q

in CIN, there is a delay of maturation/differentiation. which type of cells are occupying more of the epithelium?

A

immature basal

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29
Q

some of the nuclear abnormalities?

A

hyperchromasia, increased nucleocytoplasmic ratio, pleomorphism

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30
Q

there is excess mitotic activity situated above normal layers

A

CIN 1 - 1/3 basal occupied by abnormal cells

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31
Q

2 - abnormal cells in 2/3 and mitosis in middle third. ABNORMAL MITOTIC figures

A

in CIN3, abnormal cells occupy the full thickness of the epithelium

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32
Q

mitosis, often abnormal, in upper 1/3

A

what percentage of these progress to invasion

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33
Q

12%

A

y

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34
Q

what is the most common cervical carcinoma?

A

squamous

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35
Q

how does it develop?

A

from pre existing CIN

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36
Q

therefore why should it be preventable?

A

by screening

37
Q

symptoms of invasive cervical carcinoma?

A

usually none, abnormal bleeding, (post coital, post menopausal, BROWNISH or BLOODSTAINED vaginal discharge, contact bleeding)

38
Q

what sort of pain would you get>=?

A

pelvic pain

39
Q

why would you get haematuria?

A

local spread to ureter

40
Q

why would it lead to renal failure?

A

causes ureteric obstruction

41
Q

how can it spread?

A

local, blood, lymph

42
Q

CGIN - what is it?

A

cervical glandular intraeputhelial neoplasia

43
Q

where is its origin?

A

endocervical epithelium

44
Q

what is it a pre invasive phase of?

A

endovervical adenocarcinoma

45
Q

CGIN PRADA, why is screening of adenocarcinoma les effective?

A

difficult to diagnose pre invasive adenocarcinoma of the endocervix

46
Q

adenocarcinoma has an increased incidence in what age group?

A

young women

47
Q

although overall it is less common

A

y

48
Q

which has a better prognosis, squamous or aden?

A

squamous

49
Q

what HPV is adenocarcinoma associated with?

A

18

50
Q

what else is it associated with?

A

smoking

51
Q

makes up what percentage of cervical cancer?

A

15-25%

52
Q

commoner in young women of higher social class with later SA

A

y

53
Q

vulval HPV, whats it like in young women?

A

multifocal/recurrent/persitent, causing tx problems

54
Q

in older people, there is a greater risk of progression to invasive squamous carcinoma

A

y

55
Q

vulvar invasive squamous carcinoma - usually which age group?

A

usually elderly with ulcer or exophytic mass

56
Q

how can it arise?

A

from epithelium or VIN

57
Q

what is the most important prognostic factor?

A

spread to the inguinal lymph nodes

58
Q

treatment?

A

radical vulvectomy and lympadenectomy

59
Q

vulvar pages disease?

A

crusting rash, tumour cells in the epidermis ,contain mucin

60
Q

most of the time where does this arise from?

A

sweat gland in skin, mostly non underlying cancer

61
Q

crusting rash on vulva, contains mucin, arises from sweat gland

A

vulvar pagets disease

62
Q

what HOV involved in vulvar warts?

A

HPV 6 and 11

63
Q

squamous carcinoma of the vagina, disease of the elderly

A

y

64
Q

what is cervical ectropion?

A

increased oestrogen results in larger area of columnar epithelium in ectocervix. as its glandular, you get post coital bleeding and discharge

65
Q

which fibres carry pain from annexe/uterus/vagina?

A

visceral afferents

66
Q

from the perineum?

A

somatic sensory

67
Q

the superior aspect of pelvic organs (touching peritoneum). visceral afferents run alongside?

A

sympathetic fibres

68
Q

where do they enter the spinal cord?

A

T11-L2

69
Q

what is pain from here perceived as?

A

suprapubic

70
Q

inferior parts of pelvic organs (NOT TOUCHING PERITONEUM) run along side?

A

parasympathetic fibres

71
Q

where is pain perceived?

A

perineum

72
Q

what level does it go to?

A

S2, 3 and 4

73
Q

above the elevator ani, visceral afferents..parasympathetic s2,3,4

A

below levator ani, somatic sensory, s2,3,4, pudendal nerve, localised pan within the perineum

74
Q

when does the spinal cord become the caudal equine?

A

L2

75
Q

epidural - where is anaesthetic injected?

A

l3-l5 region

76
Q

what is epidural space made up of?

A

fat and veins

77
Q

where do sympathetic nerves exit spinal chord?

A

t1-l2

78
Q

what do all spinal nerves contain?

A

sympathetic fibres

79
Q

what do sympathetic fibres supply?

A

all arterioles (sympathetic tone)

80
Q

in spinal anaesthetic you get vasodilation

A

y

81
Q

what physical signs would you see?

A

skin look flushed, warm lower limbs, reduced sweating

82
Q

what are all these a sign of?

A

spinal anaesthetic is working

83
Q

pudendal nerve is a branch of which plexus?

A

sacral

84
Q

bloccking pudendal nerve affects?

A

majority of perineum

85
Q

which ligament does the pudendal nerve cross

A

lateral aspect of sacrospinous ligament (ischial spine can be used as a landmark)

86
Q

when would this be done?

A

painful delivery - during labour

87
Q

if baby is rhesus positive, why would future pregnancies be at risk?

A

rhd antigens could enter mothers circulation at delivery, mother mounts attack against these. antibodies could cross placenta in future pregnancies and cause homeless in fetus

88
Q

what is sensitisation?

A

when a rhd negative woman is exposed to rhd positive blood and has an immune response to it

89
Q

what do anti d antibodies given do?

A

neutralise any rhd positive antibodies that may have entered mothers circulation