(47) Diseases of the reproductive system 2 Flashcards

1
Q

What is endometriosis?

A

A condition where endometrial tissue is found outside of the uterus (ectopic endometrium)

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2
Q

What are the different theories as to why endometriosis occurs?

A
  • regurgitation theory
  • metaplasia theory
  • stem cell theory (stem cells themselves turn into endometrium)
  • metastasis theory (spread through lymphatics or vasculature)
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3
Q

In general, what does ectopic endometrium lead to?

A

Bleeding into tissues and fibrosis

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4
Q

Who does endometriosis occur in?

A

6-10% of women, 30-40 years old

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5
Q

What are the signs/symptoms of endometriosis?

A
  • 25% asymptomatic
  • dysmenorrhoea
  • dyspareunia
  • pelvic pain
  • subfertility
  • pain on passing stool
  • dysuria
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6
Q

What is dyspareunia?

A

Pain on sexual intercourse

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7
Q

What is the investigation technique into endometriosis?

A

Laparoscopy

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8
Q

What does treatment choice for endometriosis (and many other conditions) depend upon?

A

The patient’s age and whether or not they want to maintain fertility

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9
Q

What are the medical treatments for endometriosis?

A
  • COCP
  • GnRH agonists/antagonists
  • progesterone antagonists
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10
Q

What are the surgical treatments for endometriosis?

A
  • ablation

- TAH-BSO

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11
Q

What is ablation?

A

The surgical removal of body tissue

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12
Q

What is a TAH-BSO?

A

Total Abdominal Hysterectomy Bilateral Salpingo Oophorectomy

  • removes the uterus including the cervix and the ovaries including the fallopian tubes
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13
Q

What other conditions is endometriosis also linked to?

A
  • ectopic pregnancy
  • ovarian cancer
  • IBD
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14
Q

What does COCP stand for?

A

Combined oral contraceptive pill

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15
Q

What is endometritis?

A

Inflammation of the endometrium

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16
Q

What may acute endometritis be due to?

A
  • retained product of conception (POC)/placenta
  • prolonged ROM
  • complicated labour
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17
Q

What do you see on histology in acute endometritis?

A

Lots of neutrophils (manifestation of acute inflammatory response)

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18
Q

What may chronic endometritis be due to?

A
  • pelvic inflammatory disease (PID)
  • retained gestational tissue
  • endometrial TB
  • IUCD infection
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19
Q

What do you see on histology in chronic endometritis?

A

Lymphocytes and plasma cells

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20
Q

What are the signs/symptoms of endometritis?

A
  • abdominal/pelvic pain
  • pyrexia
  • vaginal discharge
  • dysuria
  • abnormal vaginal bleeding
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21
Q

What investigations are done into endometritis?

A
  • biochemistry/microbiology

- ultrasound scan (USS)

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22
Q

What is the treatment for endometritis?

A
  • analgesia
  • antibiotics
  • remove cause (eg. remove infected uterine device/retained POC etc)
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23
Q

What are endometrial polyps?

A

Sessile/polypoid E2-dependent uterine overgrowths (growths from endometrium)

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24
Q

Who do endometrial polyps occur in?

A

Less than 10% of women (40-50s)

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25
Q

How big are endometrial polyps?

A

Normally 0.5-3cm in size

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26
Q

What are the signs/symptoms of endometrial polyps?

A
  • often asymptomatic
  • intermenstrual bleeding
  • post-menopausal bleeding
  • menorrhagia
  • dysmenorrhoea

Very common cause of abnormal bleeding!

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27
Q

What are the investigations into endometrial polyps?

A
  • USS

- hysteroscopy (camera up into uterus)

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28
Q

There is a link between endometrial polyps and which drug?

A

Tamoxifen

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29
Q

What are medial treatments for endometrial polyps?

A
  • P4 (progesterone)

- GnRH agonists

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30
Q

What are the surgical treatments for endometrial polyps?

A

Curettage

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31
Q

What is curettage?

A

The use of a curette to remove tissue by scraping or scooping - used in the treatment of endometrial polyps

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32
Q

What is the prognosis for endometrial polyps?

A

Less than 1% turn malignant

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33
Q

What is leiomyomata?

A

Uterine fibroids

Benign myometrial tumours with E2/P4-depedent growth

A benign smooth muscle neoplasm

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34
Q

Who does leimyomata/uterine fibroids occur in?

A

20% of women, 30-50s

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35
Q

Why do uterine fibroids tend to regress after menopause?

A

As they are very responsive/dependent on oestrogen and progesterone

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36
Q

What are the risk factors for leiomyomata/uterine fibroids?

A
  • genetics
  • nullparity
  • obesity
  • PCOS
  • HTN
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37
Q

What is nullparity?

A

Not having any children

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38
Q

What are the signs/symptoms of leiomyomata?

A
  • often asymptomatic
  • menometrorrhagia
  • symptoms of Fe def. anaemia eg. tiredness, SOB
  • subfertility/pregnancy problems
  • pressure symptoms eg. constipation, pain on defeacation
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39
Q

What is menometrorhagia? (symptom of leiomyomata)

A

A condition in which prolonged or excessive uterine bleeding occurs irregularly and more frequently than normal - leads to iron deficient anaemia

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40
Q

What are the investigations into leiomyomata?

A
  • bimanual examination

- USS

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41
Q

What are the medical treatments for leiomyomata/uterine fibroids?

A
  • IUS
  • NSAIDs
  • OCP
  • P4
  • Fe2+
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42
Q

What are the non-medical treatments for leimyomata/uterine fibroids?

A
  • artery embolisation (using an embolus to block the artery that provides the fibroid with blood)
  • ablation
  • TAH
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43
Q

What is the prognosis for leiomyomata/uterine fibroids?

A
  • menopausal regression

- malignancy risk 0.01%

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44
Q

What does the treatment choice for uterine fibroids depend on?

A

How problematic the condition is, how close to menopause the woman is, whether she wants fertility to be maintained

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45
Q

What is endometrial hyperplasia?

A

Excessive endometrial proliferation (increased oestrogen and decreased progesterone)

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46
Q

What are the risk factors for endometrial hyperplasia?

A
  • obesity
  • exogenous E2
  • PCOS
  • E2-producing tumours
  • tamoxifen
  • HNPCC (PTEN mutations)
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47
Q

Why is obesity a risk factor for endometrial hyperplasia?

A

As there is an increase in circulating oestrogens in obesity

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48
Q

What are the different types of endometrial hyperplasia?

A

WHO classification

  • non-atypical hyperplasia
  • atypical hyperplasia
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49
Q

How many endometrial hyperplasia cases progress to carcinoma?

A

non-atypical hyperplasia = 1-3% progress

atypical hyperplasia = 23-48% are carcinoma on hysterectomy

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50
Q

What are the symptoms of endometrial hyperplasia?

A

Abnormal bleeding - IMB/PCB/PMB

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51
Q

What are the investigations into endometrial hyperplasia?

A
  • USS

- hysteroscopy +/- biopsy

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52
Q

What are the medical treatments for endometrial hyperplasia?

A
  • IUS

- P4 (progesterone)

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53
Q

What are the surgical treatments for endometrial hyperplasia?

A
  • TAH
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54
Q

What is the prognosis in endometrial hyperplasia?

A
  • endometrial adenocarcinoma

- regression

55
Q

Describe the stages in the malignant progression of hyperplasia

A
  • normal
  • non-atypical hyperplasia
  • typical hyperplasia
  • endometroid carcinoma
56
Q

Describe non-atypical hyperplasia

A

Overgrowth of whole endometrium with simple tubular glands. Varied size and shape, may be dilated. Increased gland to stroma ratio

57
Q

Describe atypical hyperplasia

A

Complex patterns of proliferating glands with nuclear atypia. Increased number of mitoses

58
Q

What is the most common cancer of the female gentile tract?

A

Endometrial carcinoma

59
Q

How often does endometrial carcinoma occur?

A

8500 new cases/2000 deaths per year in the UK

60
Q

What are the signs/symptoms of endometrial carcinoma?

A
  • PMB/IMB

- pain if late

61
Q

What are the investigations into endometrial carcinoma?

A
  • USS
  • biopsy
  • hysteroscopy
62
Q

What staging system is used in endometrial carcinoma?

A

FIGO (1-4)

63
Q

What are the medical treatments for endometrial carcinoma?

A
  • P4 (progesterone)
64
Q

What are the surgical treatments for endometrial carcinoma?

A
  • TAH-BSO

- adjuvant therapy (chemotherapy, radiotherapy)

65
Q

What is the prognosis for endometrial carcinoma?

A

stage 1 = 90% 5 year survival

stage 2-3 =

66
Q

What is type 1 endometrial carcinoma also called/described as?

A

Endometroid (75% of cases)

67
Q

What is type 2 endometrial carcinoma also called/described as?

A

Serous (25% of cases)

68
Q

At what age do types 1 and 2 endometrial carcinoma occur?

A

type 1 = pre-/perimenopausal

type 2 = postmenopausal

69
Q

What is the pre-existing stage in types 1 and 2 endometrial carcinoma?

A

type 1 = endometrial hyperplasia

type 2 = endometrial atrophy

70
Q

What are the mutations in type 1 and type 2 endometrial carcinoma?

A

type 1 = PTEN, Kras

type 2 = P53

71
Q

What is the E2 status in types 1 and 2 endometrial cancer?

A

type 1 = E2 +ve

type 2 = E2 -ve (unresponsive to oestrogen)

72
Q

What are different grades of type 1 and 2 endometrial carcinoma?

A

type 1 = can be grade 1, 2 or 3

type 2 = only grade 3

73
Q

What does PCOS stand for?

A

Polycystic ovary syndrome

74
Q

What is polycystic ovary syndrome?

A

A complex endocrine disorder, with 3 main features…

75
Q

What are the 3 main features of polycystic ovary syndrome?

A
  • hyperandrogenism
  • menstrual abnormalities
  • polycystic ovaries
76
Q

Who does PCOS affect?

A

6-10% of women (20-30% have polycystic ovaries)

77
Q

What are the investigations into PCOS?

A
  • USS
  • fasting biochemical screen (decreased FSH, increased LH, testosterone and DHEAS)
  • oral glucose tolerance test (OGTT)
78
Q

OGTT is a test for diabetes. Why is it done in suspected PCOS?

A

PCOS is associated with diabetes

79
Q

What is the diagnostic criteria for PCOS?

A

Rotterdam criteria

2/3 of - polycystic ovaries, hyperandrogenism (hirsuitism/biochemical), irregular periods (>35 days)

80
Q

What is a lifestyle change than can treat PCOS?

A

Weight loss - since polycystic ovary syndrome occurs in patients who are overweight

81
Q

What are the medical treatments for polycystic ovary syndrome?

A
  • metformin
  • OCP
  • clomiphene
82
Q

Why is clomiphene used in the treatment of PCOS?

A

Clomiphene stimulates ovulation

83
Q

What is a surgical treatment for polycystic ovary syndrome?

A

Ovarian drilling (stimulates ovaries)

84
Q

Polycystic ovary syndrome has links to which other conditions?

A
  • infertility (as not ovulating regularly, and having irregular periods)
  • endometrial hyperplasia/adenocarcinoma
85
Q

What is primary failure of the gonads called?

A

Hypergonadotrophic hypogonadism

86
Q

What hormone changes are there in hypergonadotrophic hypogonadism?

A

Raised FSH and LH (trying to compensate, but it is the gonads themselves that have failed and are unresponsive)

87
Q

What are the congenital causes of hypergonadotrophic hypogonadism?

A
  • Turner syndrome (XO)

- Klinefelter’s syndrome (XXY)

88
Q

What are the acquired causes of hypergonadotrophic hypogonadism?

A
  • infection
  • surgery
  • chemo-radiotherapy
  • toxins/drugs
89
Q

What is hypogonadotrophic hypogonadism?

A

Hypothalamic or pituitary failure causing low FSH and LH - secondary failure of the gonads

90
Q

What are the potential causes of hypogonadotrophic hypogonadism?

A
  • Sheehan’s syndrome
  • pituitary tumours
  • brain injury
  • empty sella syndrome
  • PCOS
91
Q

What is empty sella syndrome?

A

Where the pituitary gland shrinks or becomes flattened, filling the sella turcica with cerebrospinal fluid on imaging instead of the normal pituitary

92
Q

What is Sheehan’s syndrome?

A

Hypopituitarism caused by ischemic necrosis due to blood loss and hypovolemic shock during and after childbirth

93
Q

How does gonadal failure present?

A
  • amenorrhoea/absent menarche
  • delayed puberty
  • decreased sex hormone levels
  • +/- increased LH and FSH levels
94
Q

What investigations are done into gonadal failure?

A
  • hormonal profiling

- karyotyping (to rule out congenital causes)

95
Q

What are the 3 main general types of ovarian neoplasms?

A
  • surface epithelial stromal tumours
  • germ cell tumours
  • sex-cord stromal tumours
96
Q

What is the most common type of ovarian neoplasm? (90%)

A

Epithelial tumours

97
Q

What are the 3 major histological types of epithelial tumours?

A
  • serous (tubal)
  • mucinous (endocervical)
  • endometroid (endometrium)

(also transitional cell and clear cell)

98
Q

Each type of epithelial tumours has what variants?

A

Benign, borderline and malignant variants

99
Q

Describe how benign epithelial tumours are further subclassified

A

Subclassified based on components

  • cystic = cytadenomas
  • fibrous = adenofibromas
  • cystic and fibrous = cystadenofibromas
100
Q

What are malignant epithelial tumours called?

A

Cystadenocarcinomas, eg. serous cystadenocarcinoma

101
Q

What makes up around 15-20% of all ovarian tumours?

A

Germ cell tumours

102
Q

Germ cell tumours are classified into which 2 types?

A
  • germinomatous

- non-germinomatous

103
Q

What is a germinomatous germ cell tumour called?

A

Dysgerminoma

104
Q

What are the features of dysgerminoma?

A
  • differentiation towards oogonia
  • malignant
  • responsive to chemo
105
Q

Name 3 non-germinomatous germ cell tumours

A
  • teratomas
  • yolk sac tumours
  • choriocarcinomas
106
Q

What are the features of teratomas?

A
  • differentiation towards multiple germ layers
  • mature = benign, dermoid cysts, 1% malignant transformation
  • immature = malignant, often contain embryonal/immature foetal tissue
107
Q

What are the features of yolk sac tumours?

A
  • differentiation towards extraembryonic yolk sac
  • malignant
  • responsive to chemo
108
Q

What are the features of choriocarcinomas?

A
  • differentiation towards placenta
  • malignant
  • often unresponsive to chemo
109
Q

What are the treatments for germ cell tumours?

A
  • surgery
  • chemotherapy
  • radiotherapy
110
Q

Where do sex cord stromal tumours arise from?

A

Arise from the ovarian stroma, which was derived from the sex cord of the embryonic gonad (rare)

111
Q

In general, what can sex cord stromal tumours generate?

A

Cells from the opposite sex

112
Q

Name 3 types of sex cord stromal tumours

A
  • thecoma/fibrothecoma/fibroma
  • granulosa cell tumours
  • sertoli-leydig cell tumours
113
Q

What do themocas produce?

A

Benign, thecomas and fibrothecomas produce E2 (also rarely androgens)

Fibromas are hormonally inactive

114
Q

What are thecomas comprised of?

A

Spindle cells (plump spindle cells with lipid droplets = thecoma appearance)

115
Q

What is Meig’s syndrome?

A

A triad of ascites, pleural effusion/right sided hydrothorax and benign ovarian tumour

116
Q

What do granulosa cell tumours produce?

A

E2

117
Q

Are granulosa cell tumours benign or malignant?

A

Low grade malignant

118
Q

What do Sertoli-Leydig cell tumours produce?

A

Androgens

119
Q

Are Sertoli-Leydig cell tumours benign or malignant?

A

10-25% malignant

120
Q

Thecoma, fibrothecoma, fibroma and granulosa cells are all what?

A

Cells found in the normal ovary - therefore produce oestrogen

121
Q

What are sertoli cells and leydig cells?

A

Sertoli cells = produce sperm, responsive to FSH

Leydig cells = produce testosterone, responsive to LH

Normally male-derived

122
Q

How common is ovarian cancer in general?

A

2nd commonest gynae cancer

7,100 women, 4,300 deaths per year in UK

80% = >50
80-90% = epithelial
123
Q

What are the risk factors for ovarian cancer?

A
  • FH
  • increasing age
  • PMH breast cancer
  • smoking
  • E2-only HRT
  • Lynch II syndrome
  • obesity (weak)
  • nulliparity (weak)
124
Q

What are the protective factors against ovarian cancer?

A
  • OCP
  • breastfeeding
  • hysterectomy
125
Q

What are the signs/symptoms of ovarian cancer?

A
  • pain
  • bloating
  • weight loss
  • PV bleeding
  • urinary frequency
  • anorexia
126
Q

How is ovarian cancer staged?

A

FIGO staging 1-4

127
Q

What are the treatments for ovarian cancer?

A
  • TAH/BSO
  • omentectomy
  • appendectomy
  • lymphadenectomy
  • adjuvant chemotherapy
  • chemo only in sensitive germ cell tumours
128
Q

What is the prognosis in ovarian cancer?

A

Overall 5 years 43% survival

129
Q

What are the 2 categories of ovarian metastatic tumours?

A
  • Mullerian tumours (most common)

- extra-Mullerian tumours

130
Q

What are the types of Mullerian ovarian metastatic tumours?

A
  • uterus
  • fallopian tube
  • pelvic peritoneum
  • contralateral ovary
131
Q

What are the types of extra-Mullerian ovarian metastatic tumours?

A
  • GI tract (large bowel, stomach = Krukenberg tumour, pancreatobiliary
  • breast
  • melanoma
  • kidney and lung (less common)
132
Q

What are the pathways of metastasis from other sites to the ovary?

A
  • lymphatic or haematogenous spread

- direct extension from the bladder or rectum

133
Q

What is the prognosis for ovarian metastatic tumours?

A
  • tumours are confirmed histologically

- the prognosis is typically poor