Gynaecology Flashcards

1
Q

Define post-menopausal bleeding.

A

Bleeding more than 1 year after cessation of periods.

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2
Q

Define heavy menstrual bleeding.

A

Blood loss of > 80mL per period. As this is difficult to quantify, it is usually taken as whatever the patient regards as abnormally heavy.

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3
Q

What proportion of women of reproductive age suffer from heavy menstrual bleeding?

A

20-30%.

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4
Q

What are the common causes of heavy menstrual bleeding?

A
Fibroids
Adenomyosis
Endometrial polyps
Coagulation disorders
Pelvic inflammatory disease
Thyroid disease
Drug therapy (e.g. warfarin)
Intrauterine devices
Endometrial/cervical carcinoma
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5
Q

Name a diagnosis of exclusion associated with heavy menstrual bleeding.

A

Bleeding of endometrial origin (BEO).

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6
Q

What are the indications to perform endometrial biopsy in a patient reporting heavy menstrual bleeding? (5)

A
PMB and endometrial thickness on TVUSS > 4mm
HMB > 45 years
HMB associated with IMB
Treatment failure
Prior to ablative techniques
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7
Q

What are the medical management options for heavy menstrual bleeding? (4)

A

Levonorgestrel intrauterine system (LNG-IUS, Mirena) - requires long-term use, not suitable for women wishing to conceive.

Tranexamic acid - taken during menstruation.

Norethisterone - 15mg/day from day 6-26 of menstrual cycle.

GnRH agonists - stop production of oestrogen, causing amennorhoea. Only used short-term due to osteoporosis risk.

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8
Q

What are the surgical management options for heavy menstrual bleeding? (5)

A

Endometrial ablation
Uterine artery embolisation (useful for HMB associated with fibroids)
Myomectomy (useful for large fibroids causing pressure symptoms in women who wish to conceive)
Transcervical resection of fibroid (appropriate for women wishing to conceive)
Hysterectomy (useful for large fibroids causing pressure symptoms)

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9
Q

What is the medical management for acute heavy menstrual bleeding?

A
Tranexamic acid (oral or IV)
High-dose progestogens to arrest bleeding
Consider suppression with GnRH or ulipristal acetate
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10
Q

What are the causes of secondary dysmenorrhoea?

A

Endometriosis or adenomyosis
Pelvic inflammatory disease
Cervical stenosis and haematometra (rare)

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11
Q

When should diagnostic laparoscopy be performed to investigate dysmenorrhoea? (3)

A

When the history suggests endometriosis
When swabs and ultrasound scans are normal but symptoms persist
When the patient wants a definitive diagnosis or wants reassurance

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12
Q

The gonads originate from…

A

…the genital ridge overlying the embryonic kidney in the intermediate mesoderm during the 4th week of life.

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13
Q

Gonads remain sexually indifferent until when?

A

The 7th week.

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14
Q

Which gene causes the undifferentiated gonads to develop into testes?

A

the SRY gene.

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15
Q

As gonads become testes, which 2 types of cell do they differentiate into? What do these cells do?

A

Sertoli cells - produce anti-Mullerian hormone (AMH)

Leydig cells - produce testosterone

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16
Q

Which hormone surpassed development of the Mullerian ducts in males?

A

Anti-Mullerian hormone.

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17
Q

Which hormone stimulates the Wolffian ducts to develop into the vas deferens, epididymis and seminal vesicles?

A

Testosterone.

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18
Q

Which hormone causes the conversion of testosterone to DHT in the external genital skin to virile the external genitalia?

A

5-alpha reductase.

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19
Q

Development of the male genitalia: The ____ ____ becomes the penis and the _____ _____ fuse to form the scrotum. The _____ _____ fuse along the ventral surface of the penis and enclose the urethra.

A

Development of the male genitalia: The genital tubercle becomes the penis and the labioscrotal folds fuse to form the scrotum. The urogenital folds fuse along the ventral surface of the penis and enclose the urethra.

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20
Q

In the primitive ovary, which cells surround the germ cells and form primordial follicles?

A

Granulosa cells.

NOTE: Each follicle consists of an oocyte within a single layer of granulosa cells.

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21
Q

Development of the female sexual organs: Thecal cells develop from the proliferating ____ ____ and are separated from granulosa cells by the ____ ____.

A

Development of the female sexual organs: Thecal cells develop from the proliferating coelomic epithelium and are separated from granulosa cells by the basal lamina.

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22
Q

What is the maximum number of primordial follicles and when is this number reached?

A

6-7 million, reached at 20 weeks.

NOTE: By birth this is just 1-2 million (due to atresia), and by menarche 300,000-400,000 remain.

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23
Q

Development of the female sexual organs: The proximal 2/3 of the vagina develop from what?

A

The paired Mullerian ducts.

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24
Q

What forms the Fallopian tubes?

A

The unpaired caudal sections of the Mullerian ducts.

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25
Q

Development of the female sexual organs: Cells from the upper part of the urogenital sinus proliferate to produce what?

A

The sinovaginal bulbs.

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26
Q

Development of the female sexual organs: Cloacal folds fuse anteriorly to become what? What does this later develop into?

A

They become the genital tubercle, which later becomes the clitoris.

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27
Q

Development of the female sexual organs: The cloacal folds anteriorly are called what? What do these form?

A

The urethral folds - these form the labia minora.

NOTE: Another pair of folds within the cloacal membrane forms the labioscrotal folds which form the labia majora.

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28
Q

Which part of the vulva contains sebaceous and sweat glands?

A

The labia majora.

NOTE: The labia majora also contain fatty tissue at the deepest parts. The labia minora contain sebaceous glands but no adipose tissue.

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29
Q

The labia minora divide anteriorly to form which 2 structures of the vulva?

A

The prepuce

The clitoral hood (frenulum of the clitoris)

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30
Q

The labia minora divide posteriorly to form which structure of the vulva?

A

The fourchette.

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31
Q

The clitoris is made up of paired columns of erectile and vascular tissue called what?

A

The corpora cavernosa.

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32
Q

What is the function of the Bartholin’s glands?

A

They contribute to lubrication during intercourse.

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33
Q

What is the medical name for any tags remaining after perforation of the hymen?

A

Carunculae myrtiformes.

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34
Q

What type of epithelium lines the vagina?

A

Stratified squamous epithelium.

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35
Q

The vagina has no glands - how it is kept moist?

A

By secretions form the uterine and cervical glands and by transudation from the epithelial lining.

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36
Q

Why does the vagina have no glycogen before puberty or after menopause?

A

Lack of stimulation by oestrogen.

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37
Q

Name the normal vaginal commensal that breaks down glycogen to form lasting acid, producing a low pH (which protects against growth of bacteria).

A

Doderlein’s bacillus.

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38
Q

The parametrium is formed by which 2 sets of ligaments?

A

The cardinal and uterosacral ligaments.

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39
Q

How much does the adult uterus weigh?

A

70g

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40
Q

What is meant by the term cornu?

A

The site of insertion of a Fallopian tube into the uterus.

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41
Q

What are the 3 layers of the uterus?

A

Peritoneum - the outer serous layer
Myometrium - the middle muscular layer
Endometrium - the inner mucous later

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42
Q

The endometrial layer of the uterus is lined by a single layer of what form of epithelium?

A

Columnar epithelium.

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43
Q

Roughly how long is the adult cervix?

A

2.5cm

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44
Q

What is the name of the layer of connective tissue lateral to the cervix?

A

The parametrium.

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45
Q

What is the name if the anterior and posterior columns of the endocervix from which folds radiate out?

A

Arbour vitae.

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46
Q

What does the endocervix secrete?

A

Clear, alkaline mucus - this is the main component of physiological vaginal discharge.

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47
Q

What types of epithelia are found on the endocervix?

A

The epithelium of the endocervix is columnar and ciliated in the upper 2/3, and transitions to squamous at the squamocolumnar junction.

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48
Q

Where do the Fallopian tubes open up into the peritoneal cavity?

A

At the abdominal ostium.

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49
Q

What is the function of the Fallopian tubes?

A

They take the ovum from the ovary to the uterus and promote oxygenation and nutrition for sperm, ovum and zygote.

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50
Q

The Fallopian tubes run in the upper margin of the broad ligament, otherwise known as the what?

A

Mesosalpinx.

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51
Q

How long are the Fallopian tubes?

A

Roughly 10cm.

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52
Q

What are the four parts of the Fallopian tubes?

A

Interstitial portion - lies within the wall of the uterus
Isthmus - narrow portion adjoining the uterus
Ampulla - widest and longest part
Infundibulum or fimbrial portion - opening of the tube into the peritoneal cavity

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53
Q

What is the name of the longitudinal folds in the epithelia of the Fallopian tubes?

A

Plicae.

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54
Q

What are the 2 cell types in the epithelia of the Fallopian tubes?

A
Ciliated cells (produce constant current of fluid in the direction of the uterus)
Secretory cells (contribute to volume of tubal fluid)
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55
Q

What attaches the ovary to the cornu of the uterus?

A

The ovarian ligament.

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56
Q

Describe the structure of an ovary.

A

It has a central vascular medulla consisting of loose connective tissue containing elastin fibres and non-striated muscle cells
It has an outer thicker cortex which is denser than the medulla
It contains networks of reticular fibres and fusiform cells
The surface of the ovaries has a single layer of cuboidal cells (germinal epithelium)
Underneath this layer is another layer called the tunica albuginea (increases in density with age)

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57
Q

After puberty, some primordial follicles become Graafian follicles and ovulate to become the corpus luteum. This will then undergo atresia to become what?

A

Corpora albicans.

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58
Q

What is the arrangement of muscle in the bladder?

A

An inner longitudinal layer, a middle circular layer and an outer longitudinal layer.

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59
Q

What type of epithelium is found in the bladder?

A

Transitional epithelium.

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60
Q

What is the average bladder capacity?

A

400mL

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61
Q

The internal meatus of the urethra is known as what?

A

The trigone.

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62
Q

What separates the bladder from the anterior vaginal wall?

A

The pubocervical fascia.

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63
Q

What type of epithelium is found in the urethra?

A

Transitional epithelium.

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64
Q

How is the smooth muscle of the wall of the urethra arranged?

A

Into outer longitudinal and inner circular layers.

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65
Q

The ureter lies in front of the bifurcation of which artery?

A

The common iliac artery.

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66
Q

The blood supply of the ureter is mainly from small branches of which artery?

A

The ovarian artery.

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67
Q

The rectum begins at which vertebral level?

A

S3.

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68
Q

The rectum is separated from the posterior vaginal wall by what?

A

The rectovaginal fascial septum.

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69
Q

Which ligaments are found lateral to the rectum?

A

The uterosacral ligaments.

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70
Q

The pelvic diaphragm is formed by the levator ani muscles, and is described in 2 parts - name these parts.

A

Pubococcygeus - arises from the pubic bone and the anterior part of the tendinous arch of the pelvic fascia.

Iliococcygeus - arises from the posterior part of the tendinous arch and the ischial spine.

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71
Q

What is the urogenital diaphragm (aka the triangular ligament) and which 2 structures pierce it?

A

Two layers of pelvic fascia that fill the gap between the descending pubic rami and lie beneath the levator ani muscles.

It is pierced by the urethra and the vagina.

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72
Q

When taking a cervical smear, you put the brush into the cervical os and rotate how many times? Then, you put it into the pot and rotate how many times?

A

5x in the os

10x in the pot

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73
Q

What are the 2 types of speculum?

A

Bivalve (aka Cusco’s) - holds back the anterior and posterior walls of the vagina to allow visualisation of the cervix, and has a screw so that it can be tightened to keep it in place.

Sim’s - allows inspection of the vaginal walls, and is used in left lateral position.

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74
Q

Microbiology swabs are taken from which part of the vagina?

A

The vaginal fornices.

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75
Q

Endocervical swabs for chlamydia are taken from where?

A

The endocervical canal.

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76
Q

How is the size of the uterus described upon bimanual examination?

A

In terms of week of gestation (e.g. a 6 weeks size uterus).

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77
Q

When performing a transvaginal USS, what can be done to distend the uterine cavity and allow easier detection of abnormalities?

A

Saline instillation sonography (instilling saline through the cervix).

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78
Q

What must you always do before performing an endometrial biopsy on a woman.

A

Confirm that she is not pregnant.

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79
Q

Which hypothalamic hormone stimulates pituitary secretion of LH and FSH?

A

GnRH

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80
Q

Which cells in the hypothalamus synthesise and release LH and FSH?

A

Basophil cells.

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81
Q

How does the COCP stop the periovulatory LH surge?

A

It maintains constant oestrogen levels within the negative feedback range, preventing high levels of oestrogen in the late follicular phase which would lead to increased LH production due to increased concentrations of GnRH receptors.

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82
Q

Which 3 phases does the ovary go through during a cycle?

A

Follicular
Ovulatory
Luteal

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83
Q

What affects to LH and FSH have on the theca and granulosa cells of follicles?

A

Theca cells - LH stimulates production of androgens from cholesterol.

Granulosa cells - Convert androgens from theca cells into oestrogen via the process of aromatisation under the influence of FSH.

NOTE: Therefore, as follicles grow, oestrogen secretion increases.

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84
Q

Which 2 substances are released by granulosa cells to downregulate and upregulate FSH?

A

Inhibin - down regulates FSH release and enhances androgen synthesis.

Activin - produced by granulosa cells and the pituitary and acts to increase FSH binding on follicles.

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85
Q

How big will the dominant follicle be by the end of the follicular phase?

A

20mm diameter

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86
Q

What causes the LH surge at ovulation? (2)

A
  • Oestrogen production increases until it reaches a positive feedback threshold
  • LH-induced luteinisation of granulosa cells in the dominant follicle causes progesterone to be produced, which exerts more positive feedback for LH secretion
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87
Q

Ovulation occurs after breakdown of the follicular wall under the influence of what? (4)

A

LH
FSH
Proteolytic enzymes
Prostaglandins

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88
Q

Why should women wanting to become pregnant avoid taking PG synthetase inhibitors such as aspirin or ibuprofen?

A

Because prostaglandins are important in ovulation, so inhibiting their production can lead to anovulation.

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89
Q

Why does the corpus luteum undergo extensive vascularisation?

A

To supply granulosa cells with a rich blood supply for continued steroid production (aided by local VEGF production).

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90
Q

How long does the luteal phase last?

A

14 days.

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91
Q

Luteolysis of the corpus luteum occurs in the absence of what?

A

Beta-hCG produced by the implanting embryo.

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92
Q

What are the phases of the endometrium throughout the menstrual cycle?

A

The proliferative phase
The secretory phase
Menstruation

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93
Q

During the proliferative phase, glandular and stromal growth of the endometrium begins. The epithelium changes from a single layer of columnar cells to what type of epithelium?

A

Pseudofenestrated epithelium.

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94
Q

The endometrium enters the proliferative phase at 0.5mm thickness - how thick does it become during this phase?

A

3.5-5mm

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95
Q

During the secretory endothelial phase, what does progesterone do?

A

Induces the formation of a temporary layer (decidua) in the endometrial stroma.

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96
Q

During the secretory endothelial phase, apical membrane projection of epithelial cells appear (after day 21-22), making the endometrium more receptive for implantation. What are these projections called?

A

Pinopodes.

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97
Q

What are the 3 layers of the endometrium seen immediately before menstruation?

A

Basalis - lower 25% which remains throughout the menstrual cycle.

Stratum spongiosum - oedematous stroma and exhausted glands.

Stratum compactum - upper 25% with prominent decidualised stromal cells.

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98
Q

What causes the breakdown and loss of the upper endometrial layers during menstruation?

A

Fall in oestrogen and progesterone at the end of the luteal phase leads to loss of tissue fluid, vasoconstriction of spiral arterioles and distal ischaemia.

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99
Q

Why may people who are underweight not go through puberty?

A

Because leptin plays a permissive role in puberty, and is produced by white adipose tissue.

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100
Q

In terms of puberty, what is meant by the terms:
Thelarche
Adrenarche
Menarche

A

Thelarche - breast development
Adrenarche - pubic and axillary hair growth
Menarche - onset of menstruation

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101
Q

Which staging can be used to describe pubertal development?

A

Tanner staging.

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102
Q

Precocious puberty:
Definition
Classification

A

Definition - onset of puberty by the age of 8 in a girl, or 9 in a boy.

Classification:
Central - gonadotrophin development
Peripheral - gonadotrophin independent (this may be caused by exogenous ingestion of oestrogen or a hormone producing tumour)

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103
Q

Delayed puberty:
Definition
Causes associated with a central defect (4)
What is gonadal failure (hypergonadotrophic hypogonadism) associated with? (2)

A

Definition - when there are no signs of secondary sexual characteristics by the age of 14 years.

Causes associated with a central defect:
Anorexia nervosa
Excessive exercise
Chronic illness
Kallmann's syndrome

What is gonadal failure (hypergonadotrophic hypogonadism) associated with?
Turner syndrome
XX gonadal dysgenesis

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104
Q

List the non-structural causes of disorders of sexual development. (5)

A
Turner syndrome (45 X)
46 XY Gonadal Dysgenesis
46 XY DSD
5-Alpha Reductase Deficiency
46 XX DSD
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105
Q

Turner syndrome (45 X):
Main clinical features (3)
Associated medical conditions (5)

NOTE: In Turner syndrome, the gonads are called streak gonads and do not function to produce oestrogen or oocytes.

A

Main clinical features:
Short stature
Webbing of the neck
Wide carrying angle

Associated medical conditions:
Coarctation of the aorta
Inflammatory bowel disease
Sensorineural and conductive deafness
Renal anomalies
Endocrine dysfunction
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106
Q

What is it Swyer syndrome?

A

Complete 46 XY gonadal dysgenesis - the gonad remains as a streak and does not produce any hormones.

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107
Q

In 46 XY gonadal dysgenesis, why must the dysgenetic gonad be removed following diagnosis?

A

High malignancy risk

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108
Q

What is mixed gonadal dysgenesis also known as?

A

Ovotesticular disorder of sexual development - both functioning ovarian and testicular tissue can be present.

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109
Q

How can puberty be induced in a patient with 46 XY gonadal dysgenesis?

A

Using oestrogen.

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110
Q

46 XY DSD:
Most common cause
Why does virilisation not occur, despite normal functioning of the testes and production of AMH?
When/how does presentation usually occur?
Management (3)

A

Most common cause - complete androgen insensitivity.

Why does virilisation not occur, despite normal functioning of the testes and production of AMH?
Partial or complete inability of the androgen receptor to respond to androgen stimulation.

When/how does presentation usually occur?
At puberty with primary amenorrhoea.

Management:
Gonadectomy (due to risk of testicular malignancy)
Long-term HRT
Vaginal dilatation (to allow penetrative intercourse)

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111
Q

5-alpha reductase deficiency - how does it present and why?

A

Usually with ambiguous genitalia - this is because the foetus is XY and has functioning testes which produce both testosterone and AMH, but testosterone cannot be converted to DHT causing normal virilisation.

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112
Q

46 XX DSD:
Most common cause
Physical changes seen as a result of female virilisation (3)
Management (2)

A

Most common cause - congenital adrenal hyperplasia (CAH)

Physical changes seen as a result of female virilisation:
Enlarged clitoris
Fused labia (scrotal in appearance)
Upper vagina joins the urethra and opens as one common channel into the perineum

Management:
Lifelong steroid replacement
Surgical treatment of genitalia may be considered

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113
Q
Define:
Amenorrhoea
Primary amenorrhoea
Secondary amenorrhoea
Oligomenorrhoea
Premature ovarian failure
A

Amenorrhoea - absence of menstruation for more than 6 months in the absence of pregnancy in a woman of fertile age.

Primary amenorrhoea - when a girl fails to menstruate by 16 years of age.

Secondary amenorrhoea - absence of menstruation for > 6 months in a normal female of reproductive age that is not due to pregnancy, lactation or menopause.

Oligomenorrhoea - irregular periods at intervals of more than 35 days, with only 4-9 periods per year.

Premature ovarian failure - cessation of periods < 40 years of age.

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114
Q

What is haematocolpos?

A

Filling of the vagina with blood - this can be seen in primary amenorrhoea where Mullerian defects are present in the genital tract.

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115
Q

What is Asherman syndrome?

A

Secondary amenorrhoea caused by scarring of the endometrium.

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116
Q

When investigating amenorrhoea or oligomenorrhoea, bloods should be taken to measure hormone levels - what will be seen in a patient with:
PCOS
Premature ovarian failure

A

PCOS = raised LH and testosterone

Premature ovarian failure = raised FSH

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117
Q

Management of Asherman syndrome.

A

Adhesiolysis and IUD insertion at time of diagnostic hysteroscopy.

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118
Q

What are the diagnostic criteria for PCOS?

A

Rotterdam Consensus Criteria - must have 2 of:
Amenorrhoea/Oligomenorrhoea
Clinical or biochemical hyperandrogenism
Polycystic ovaries on USS - 12+ sub capsular follicular cysts < 10mm in diameter and increased ovarian stroma

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119
Q

Management of PCOS.

A

COCP to regulate menstruation (increases sex hormone-binding globulin which helps relieve androgenic symptoms)
Cyclical oral progesterone (regulate withdrawal bleed)
Clomiphene (SERM which can induce ovulation if subfertility is an issue)
Lifestyle advice/Weight reduction
Ovarian drilling (destroys ovarian stroma and may prompt ovulatory cycles)
Treatment of androgenic symptoms

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120
Q

Which drugs can be used to treat moderate to severe premenstrual syndrome? (4)

A

SSRIs
Transdermal oestradiol (cycle suppression)
Some COCPs (cycle suppression)
GnRH analogues

NOTE: Hysterectomy with bilateral salpingo-oophorectomy can be used as a last resort.

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121
Q

How does the implanted blastocyst maintain the thickness of the endometrium?

A

It secretes hCG which acts on the corpus luteum to rescue it from luteolysis. The corpus luteum produces progesterone which maintains the endometrium, prevents menstruation and supports the early conceptus.

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122
Q

At what stage of pregnancy does the placental tissue take over from the corpus luteum as the main supply of progesterone?

A

8 weeks.

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123
Q

What is a biochemical pregnancy?

A

A pregnancy that fails during the early stages of implantation - it will present with a transiently positive hCG (positive before expected period, but negative after).

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124
Q

The foetal heartbeat is visible as early as…

A

…6 weeks gestation.

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125
Q

Define miscarriage.

A

Pregnancy that ends spontaneously before 24 weeks gestation.

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126
Q

What are the types of miscarriage? (5)

A
Threatened miscarriage
Inevitable miscarriage
Incomplete miscarriage
Complete miscarriage
Missed miscarriage
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127
Q

Threatened miscarriage management.

A

Return for further assessment if the bleeding gets worse or persists beyond 14 days.
Continue routine antenatal care if bleeding stops.

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128
Q

Medical management of miscarriage.

A

Offer vaginal misoprostol
If bleeding has not started within 24 hours of treatment, contact a healthcare professional
Pain relief/anti-emetics

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129
Q

Surgical management of miscarriage.

A

Manual vacuum aspiration under local anaesthetic
Surgical management in theatre under GA
Vaginal/sublingual misoprostol may be used to ripen the cervix to facilitate cervical dilatation for suction insertion
Offer anti-D prophylaxis to all Rhesus negative women

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130
Q

Recurrent miscarriage:
Definition
Risk factors (5)
Causes (5)

A

Definition - loss of three or more consecutive pregnancies.

Risk factors:
Advancing maternal and paternal age
Obesity
Balanced chromosomal translocations
Uterine structural anomalies
Antiphospholipid syndrome
Causes:
Antiphospholipid syndrome
Cervical abnormalities
Foetal chromosomal abnormalities
Uterine malformations
Thrombophilia
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131
Q

Recurrent miscarriage:
Investigations
Management

A

Investigations:

  • Screen for antiphospholipid syndrome - lupus anticoagulant and anti-cardiolipin antibodies
  • Cytogenetic analysis of products of conception in last miscarriage, and of both partners’ peripheral blood
  • TVUSS - assess for uterine anomalies
  • Screen for haemophilia

Management:
Anti-phospholipid syndrome - low-dose aspirin and LMWH in future pegnancies
Consider cervical cerclage if applicable

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132
Q

Define ectopic pregnancy.

A

Implantation of a pregnancy outside the normal uterine cavity (98% occur in the Fallopian tubes).

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133
Q

Define heterotypic pregnancy. When does this occur more commonly?

A

Simultaneous development of two pregnancies, one within and one outside the uterine cavity. Incidence is higher in patients receiving IVF.

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134
Q

How does ectopic pregnancy present?

A

Abdominal pain and/or vaginal bleeding in early pregnancy.

NOTE: Rarely presents with very acute rupture of the ectopic pregnancy and massive intraperitoneal bleeding.

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135
Q

How might an ectopic pregnancy present with shoulder tip pain?

A

If patients present with rupture of the ectopic pregnancy and massive intraperitoneal bleeding, the free blood in the peritoneal cavity can cause diaphragmatic irritation and shoulder tip pain.

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136
Q

How can serum hCG help to identify ectopic pregnancy?

A

In normal pregnancies, it doubles every 48 hours, but in ectopic pregnancy, this rise in hCG is suboptimal.

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137
Q

What are the medical and surgical management options for ectopic pregnancy?

NOTE: Expectant management is used when possible, on the assumption that a significant proportion of ectopic pregnancies resolve without treatment. Only use this if the patient is haemodynamically stable and asymptomatic.

A

IM Methotrexate (if the presentation is not particularly concerning i.e. no significant pain, serum bhCG < 1500).

Anti-D prophylaxis in RhD negative women undergoing surgical management.

Surgery (if presentation is concerning i.e. significant pain, bhCG > 5000):
Laparoscopic where possible
Salpingectomy or salpingotomy

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138
Q

Define gestational trophoblastic disease.

A

A spectrum of conditions that includes complete and partial hyatidiform mole, invasive mole and choriocarcinoma.

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139
Q

Vulval vestibule:
Definition
Type of epithelium
What does it contain? (3)

A

Definition - the area between the lower end of the vaginal canal at the hymenal ring and the labia minora.

Type of epithelium - non-keratinised, non-pigmented squamous epithelium.

What does it contain?
Ducts of the minor vestibular glands
Ducts of the periurethral Skene’s glands
Ducts of the Bartholin’s glands

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140
Q

What type of epithelium lines the labia minora/majora?

A

Keratinised, pigmented, squamous epithelium.

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141
Q

Define vulvodynia.

A

Chronic vulval pain with no identifiable cause.

NOTE: It is considered neuropathic and may be treated with amitriptyline.

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142
Q

How might vulval pruritus cause dysuria?

A

If the patient itches then urine may burn the excoriated vulval skin.

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143
Q

What diagnosis should be considered in patients presenting with recurrent thrush?

A

Diabetes mellitus.

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144
Q

How should vulval candidal infection be treated?

A

1st line = 150mg clotrimazole nightly over 3 consecutive nights
2nd line = fluconazole

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145
Q

What proportion of women with vulval pruritus have low ferritin?

A

5% - correction of this will help to improve symptoms.

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146
Q

What type of biopsy is used to test for malignancy of the vulva?

A

Keyes punch biopsy.

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147
Q

Lichen Planus:
Definition
Symptoms (5)
Management (2)

A

Definition - autoimmune disorder affecting 1-2% of the population. It affects the skin, genitalia and oral and GI mucosa.

Symptoms:
Pruritus
Superficial dyspareunia
Oral lesions
Longitudinal ridging of the nailbeds
Genital lesions

Management:
High-dose topical steroids
If vaginal stenosis, dilatation with manual measures should be attempted in the first instance

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148
Q
Lichen Sclerosus:
Definition
Symptoms (4)
Management (1)
Association (1)
A

Definition - destructive inflammatory skin condition that mainly affects the anogenital area of women.

Symptoms:
Pruritus
Hypopigmentation
Loss of anatomy
Vaginal stenosis and cracking

Management:
Strong steroid ointments

Association:
Vulval cancer

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149
Q

What are the 3 types of vulval cysts?

A

Bartholin’s cysts (may become infected causing Bartholin’s abscess)
Skene gland cysts
Mucous inclusion cysts

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150
Q

What is meant by marsupialisation of a cyst?

A

Suturing the internal aspect of the cyst to the outside to prevent it from reforming.

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151
Q

What is the difference between superficial and deep dyspareunia?

A
Superficial = affecting the vagina, clitoris or labia
Deep = pain within the pelvis
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152
Q

What is the difference between primary and secondary psychosexual dysfunction?

A

Primary = sexual difficulties where there may be psychosomatic pain.

Secondary = sexual difficulties resulting from pain or emotional issues.

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153
Q

Define vaginismus.

A

Involuntary contraction of the vaginal muscles during vaginal examination (or intercourse).

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154
Q

What are the 4 degrees of female genital mutilation?

NOTE: Treatment may involve cosmetic surgery and de-infibulation.

A

Type 1 - clitoroidectomy - excision of the clitoral hood with or without removal of the clitoris.

Type 2 - excision of the clitoris and partial or total removal of the labia minora.

Type 3 - excision of part of all of the external genitalia (clitoris, labia minora and majora) and stitching/narrowinf of the vagina (infibulation).

Type 4 - piercing the clitoris, cauterisation, cutting the vagina, inserting corrosive substances. Also includes any plastic surgery procedures done as an adult.

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155
Q

Which contraceptives prevent ovulation?

A

Combined hormonal methods (pill, patch and vaginal ring)
Progesterone-only injectables
Progesterone-only implant (Nexplanon)
Oral emergency contraception

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156
Q

Which contraceptives prevent sperm reaching the oocyte?

A
Female sterilisation
Male sterilisation (vasectomy)
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157
Q

Which contraceptives prevent an embryo implanting in the uterus?

A

Cu-IUD

LNG-IUS

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158
Q

Which contraceptives block the passage of sperm beyond the vagina?

A

Diaphragm
Cap
Progestogens

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159
Q

How often does the Nexplanon implant need to be replaced?

A

Every 3 years.

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160
Q

How often are IUDs replaced?

A

Every 5-10 years.

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161
Q

What advise should you give to a woman who is using enzyme-inducing medication (e.g. anticonvulsants, antifungals, antibiotics, antiretrovirals) and wants to use hormonal methods of contraception?

A

Use condoms as well, or consider using methods that are unaffected by enzyme induction (Cu-IUD, LNG-IUS, progesterone-only injectable).

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162
Q

What is the only hormonal method of contraception that is evidenced to cause weight gain?

A

Progesterone-only injectable.

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163
Q

What does a woman need to know before starting a method of contraception? (6)

A
How to use the method and what to do when missed
Typical failure rates
Common side-effects
Health benefits
Fertility returning on stopping
When she requires review
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164
Q

What are the 3 formulations of combined hormonal contraception (oestrogen and progestogen)?

A

Oral pill
Transdermal patch
Vaginal ring

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165
Q

How do combined hormonal contraceptives work?

A

They inhibit ovulation via negative feedback of oestrogen and progestogen on the pituitary with suppression of LH and FSH.

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166
Q

Most commonly, COCPs contain _____ _____ (15-35mcg), and preparations contain ___ pills followed by a 7-day pill-free interval.

A

Most commonly, COCPs contain ethinyl oestradiol (15-35mcg), and preparations contain 21 pills followed by a 7-day pill-free interval.

NOTE: Pill-free interval causes a withdrawal bleed and there is no reason a patient cannot take the pill continuously.

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167
Q

What should women taking the COCP do if experiencing dysmenorrhoea or headaches during the pill-free interval?

A

Tricycling - take 3 packets without a break.

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168
Q

How are progestogens (found in COCPs) categorised?

A

2nd generation - levonorgestrel, norethisterone
3rd generation - gestodene, desogestrel
4th generation - drospirenone, dienogest

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169
Q

Which generations of progestogens are associated with increased risk of venous thrombosis?

A

3rd generation (gestodene, desogestrel) and 4th generation (drospirenone, dienogest).

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170
Q

How much ethinyl oestradiol and how much norelgestromin does a combined hormonal transdermal patch release per day (it is left on for 7 days, and after 21 days patients undertake a 7-day hormone-free interval)?

A

Ethinyl oestradiol - 33.9mcg

Norelgestromin - 203mcg

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171
Q

How much ethinyl oestradiol and how much etonorgestrel does the combined hormonal ring release per day (it is inserted and left for 21 days, after which patients undertake a 7-day hormone-free interval)?

NOTE: It is the lowest dose combined hormonal method of contraception.

A

Ethinyl oestradiol - 15mcg

Etonorgestrel - 120mcg

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172
Q

What is the protocol for patients who have missed one or more COCPs?

A

If one pill has been missed, take the missed pill as soon as you remember, and continue to take remaining pills at the usual time.

If > 1 piss is missed, take the missed pill as soon as you remember, and continue to take remaining pills at the usual time. Use condoms or avoid sex for the next 7 days.
In the next 3 weeks if pills are missed, consider emergency contraception and consider omitting the pill-free interval.

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173
Q

How long does the contraceptive effect of the progestogen-only injectable last?

A

14 weeks.

174
Q

How long does the contraceptive effects the progestogen-only implant last?

A

3 years.

175
Q

How does the COCP impact cancer risk?

A

12% reduced risk of any cancer
Reduced risk of colorectal, endometrial and ovarian cancer
Increased risk of breast cancer during use (back down to normal risk by 10 years after cessation)
Increased risk of cervical cancer

176
Q

Why are women > 35 years old who smoke not eligible for combined hormonal contraception?

A

Increased risk fo arterial disease with CHC.

177
Q

What are risks are associated with combined hormonal contraception? (2)

A

VTE

Arterial disease

178
Q

Why is combined hormonal contraception contraindicated in women who have migraine with aura?

A

Because migraine with aura is associated with cerebral vasospasm and women may be at increased risk of stroke if they use CHC.

179
Q

What are the 4 formulations of progestogen-only contraceptive methods?

A

Oral
Injectable
Implant
Intrauterine system

180
Q

How do progestogen-only contraceptives reduce sperm penetrability and transport?

A

By thickening cervical mucus.

181
Q

How does the LNG-IUS work?

A

Causes marked endometrial trophy meaning that implantation is not possible.

182
Q

What are the side-effects of progestogen-only pills (POPs)? (3)

NOTE: POPs need to be taken continuously.

A

Irregular bleeding
Persistent ovarian follicles (simple cysts)
Acne

183
Q

What should a woman do if they miss a progestogen-only pill?

A

Continue taking POP and use extra precautions (condoms or avoid sex) for 48 hours. If unprotected sex occurs in this time, emergency contraception is recommended.

184
Q

Which progestogen does Nexplanon (single rod progestogen-only implant) contain?

A

Etonorgestrel (released 60-70mcg per day for 3 years).

185
Q

Where is the Nexplanon implant inserted?

NOTE: There is no need for follow-up until the device is due for removal.

A

Subdermally 8cm above the medial epicondyle usually in the non-dominant arm (under local anaesthesia).

186
Q

What is the most commonly used progestogen-only injectable?

NOTE: Injection interval 12-14 weeks.

A

Depot injection of medroxyprogesterone acetate - administered as IM depoprovera (150mg) or SC Sayana press (104mg).

187
Q

How long does it take for fertility to return after discontinuation of progestogen-only injectables?

A

Up to 1 year after last injection.

188
Q

What are the 2 LNG-IUSs available in Europe and the USA?

A

52mg LNG-IUS (Mirena) - licenced for 5 years

13.5mg LNG-IUS (Jaydess) - licenced for 3 years

189
Q

What are the side-effects of LNG-IUS? (5)

A
Acne
Breast tenderness
Mood disturbance
Headaches
Unpredictable bleeding in first few months
190
Q

What are the non-contraceptive benefits of LNG-IUS? (4)

A

Reducing heavy menstrual bleeding
Treating dysmenorrhoea
Reducing pain associated with endometriosis and adenomyosis
Protecting the endometrium against hyperplasia

191
Q

How does the Cu-IUD work?

A

Stimulates inflammatory reaction in the uterus which is toxic to both sperm and egg, and inhibits implantation.

192
Q

What bleeding patterns can be expected with the LNG-IUD and the Cu-IUD?

A
LNG-IUD = lighter, less painful menses
Cu-IUD = more painful, heavier menses
193
Q

What risk should you be aware of if a patient becomes pregnant whilst using a contraceptive IUD?

A

They have an increased risk of the pregnancy being ectopic.

194
Q

IUDs should be removed before 12 weeks gestation in women who become pregnant whilst using them. What are the risks of leaving the IUD in situ?

A

Miscarriage
Preterm delivery
Septic abortion
Chorioamnionitis

195
Q

What are the risks of IUD insertion? (4)

A

Perforation - Presents with missing threads and severe pain following insertion. USS will show no IUD in the uterus.

Expulsion - 1 in 20 expel within first 3 months.

Infection - 1 in 100 in first 3 weeks. Actinomyces-like organisms (ALOs) are common.

Missing threads - May indicate pregnancy, expulsion or perforation.

196
Q

Which spermicidal product is usually sold for use with diaphragms and caps?

A

Nonoxynol 9 - may increase HIV transmission.

197
Q

What are the 3 surgical approaches to female sterilisation?

A

Laparoscopy
Hysteroscopy
Laparotomy (e.g. at C-section)

198
Q

In laparoscopic female sterilisation, ____ ____ are most commonly used to occlude the Fallopian tubes.

A

In laparoscopic female sterilisation, Filshie clips are most commonly used to occlude the Fallopian tubes.

199
Q

For how long after laparoscopic and how long after hysteroscopic female sterilisation is effective contraceptive still required?

A

Laparoscopic - until first menstrual period

Hysteroscopic - 3 months

200
Q

What risk should you be aware of in a patient who becomes pregnant despite having undergone female sterilisation?

A

Increased risk of ectopic pregnancy.

201
Q

How does a hysteroscopic sterilisation work?

A

Expanding springs (micro-inserts) are inserted into the tubal Ostia via a hysteroscope. These induce fibrosis in the corneal section of each Fallopian tube over 3 months.

202
Q

How can we check whether a vasectomy has been successful?

A

Semen analysis at 12 weeks post-op to confirm the absence of spermatozoa in the ejaculate.

203
Q

List the different fertility awareness-based methods (FABs). (5)

A
Calendar or rhythm method 
Temperature method
Cervical mucus method
Cervical palpation
Personal fertility monitor
204
Q

What is the most effective method of emergency contraception?

A

Cu-IUD - it can be inserted up to 5 days after unprotected sex or 5 days after predicated ovulation, and can then be removed once pregnancy is excluded or left in as contraception.

205
Q

What are the 2 oral methods of emergency contraception? How long are they effective for?

NOTE: Only prevent 2/3 of pregnancies.

A

Levonorgestrel (1.5mg) - effective up to 72 hours after unprotected sex.

Ulipristal acetate (30mg) - progesterone receptor modulator, effective up to 120 hours after unprotected sex.

206
Q

The 1967 Abortion Act states that abortion can be performed if 2 registered medical practitioners acting in good faith agree that pregnancy should be terminated on one of the recognised legal grounds.

What are the recognised grounds?

A

Ground A - Risk to life of pregnant woman.
Ground B - Needed to prevent serious injury to pregnant woman.
Ground C - < 24 weeks and reduce risk to pregnant woman.
Ground D - < 24 weeks and reduce risk of injury (mental/physical) to family of woman.
Ground E - Risk of handicap to child.
Ground F - Save life of pregnant woman.

207
Q

Which pre-abortion investigations are recommended?

A

Gestation assessment (USS or clinical)
Rhesus status
Consider STI testing
Consider FBC (determine whether anaemic)

208
Q

What combination of drugs is given in medical abortion? How does this work?

A

Mifepristone (progesterone receptor modulator)
Followed by misoprostol (prostaglandin analogue)

Mifepristone brings about an increase in uterine contractility and sensitises the uterus to exogenous prostaglandins. Misoprostol then brings about expulsion.

209
Q

After what stage of gestation must medical abortion take place in a clinical environment rather than at home?

A

After 9 weeks because of discomfort, increased bleeding and passage of a larger foetus.

210
Q

If abortion occurs after 21 weeks gestation, foeticide should be used to eliminate the possibility of the aborted foetus showing signs of life. How is this achieved?

A

Intracardiac infection of potassium chloride or intrafoetal/intramniotic digoxin.

211
Q

Vacuum aspiration should be used to conduct surgical termination of pregnancy up to what stage?

A

14 weeks gestation.

NOTE: Consider pre-treatment with misoprostol which causes cervical dilatation.

212
Q

What is the surgical intervention of choice for termination of pregnancy after 14 weeks?

A

Dilatation and evacuation.

213
Q

How is dilatation achieved for the dilatation and evacuation method of surgical termination of pregnancy?

A

Osmotic dilators
Misoprostol (vaginal or sublingual)
Mifepristone (oral)

214
Q

Define subfertility. What proportion of heterosexual couples does it affect?

A

Failure to conceive after 12 months of regular unprotected intercourse. It affects 1 in 7 heterosexual couples.

215
Q

For how long after ovulation do eggs remain fertilisable?

A

12-24 hours.

216
Q

How long can sperm survive in the female reproductive tract?

A

Up to 72 hours.

217
Q

How many days before menstruation does ovulation usually occur?

A

14 days.

218
Q

With regards to female subfertility, what is the most common cause of ovulatory issues?

A

PCOS.

NOTE: Hypothalamic disorders and pituitary disease are less common causes of anovulation.

219
Q

Tubal problems with female fertility are associated with inflammatory processes which block the Fallopian tubes. Give 3 causes.

A

Pelvic inflammatory disease (particularly infection with chlamydia)
Endometriosis
Previous pelvic or abdominal surgery (scar tissue/adhesions)

220
Q

Which type of fibroids are most likely to cause failure of implantation, leading to female subfertility?

A

Submucosal fibroids.

NOTE: Intramural fibroids may reduce fertility if large, but subserosal fibroids have little impact.

221
Q

List the causes of male subfertility. (6)

A

Reduction in sperm count and quality
Spermatogonial cells damaged by inflammation or damage to epididymis (responsible for storing sperm)
Pelvic radiotherapy/surgery
Diabetes mellitus
Erectile difficulties/problems with ejaculation
Aneuploidy of sex chromosomes

222
Q

When investigating subfertility, which hormones will you look at when performing a blood hormone profile? (3)

A

Early follicular phase FSH, LH and oestradiol
Anti-Mullerian hormone (AMH) for assessing ovarian reserve (it is independent of the menstrual cycle)
Mid-luteal progesterone (to confirm ovulation)

NOTE: If irregular cycle, also consider assessing TFTs, prolactin and testosterone.

223
Q

Which viruses should be screened for if considering assisted reproductive technology (ART) to treat subfertility? (3)

A

HIV
Hepatitis B
Hepatitis C

224
Q

What can be used to predict response to assisted reproductive technology (ART)?

A

Ovarian reserve - a good indicator for this is antral follicle count (AFC) on TVUSS.

< 4 = poor response
16+ = good response

NOTE: AMH is the most successful biomarker of ovarian reserve as it does not change in response to gonadotrophins.

225
Q

How is tubal assessment usually performed when assessing subfertility?

A

Hysterosalpingography (HSG) using X-ray or ultrasound.

NOTE: Tubal patency does not indicate tubal function.

226
Q

What is the main subfertility investigation for males?

A

Semen fluid analysis (SFA).

227
Q

What does semen fluid analysis assess? (7)

A
Volume
Sperm concentration
Total sperm number
Mortality
Morphology
Vitality
pH
228
Q

For how long should a patient abstain from ejaculation before providing a semen sample?

A

2-4 days.

229
Q

If semen fluid analysis (SFA) is abnormal upon initial investigation, how long should you wait to repeat it and why?

A

3 months, because SFA can be distorted by viral infection.

230
Q

If semen fluid analysis (SFA) identifies low sperm count or azoospermia, what test should be performed?

A

Hormone profile.

231
Q

What are the medical options for the treatment of subfertility? (5)

A

Ovulation induction with clomiphene or FSH
Intrauterine insemination (with/without stimulation with FSH)
Donor insemination (with/without stimulation with FSH)
IVF
Donor egg with IVF

232
Q

What are the surgical options for the treatment of subfertility? (4)

A

Operative laparoscopy to treat disease/restore anatomy (adhesions, endometriosis, ovarian cyst)

Myomectomy (for uterine fibroids)

Tubal surgery

Laparoscopic ovarian drilling (PCOS unresponsive to medical management)

233
Q

What is the first line option for patients with PCOS-related ovulatory problems?

A

Ovarian induction.

234
Q

What is the most commonly used ovarian induction agent? How does it work?

A

Clomiphene citrate.

It is an anti-oestrogen which binds to oestrogen receptors in the hypothalamus and pituitary, blocking negative feedback exerted by oestrogen. This causes a surge in gonadotrophin release, which stimulates the ovary to recruit more follicles for maturation.

235
Q

When treating PCOS-related ovulatory problems, what are the options for clomiphene-resistant women? (4)

A

Augmentation with metformin
Aromatase inhibitors
Injectable gonadotrophins
Laparoscopic ovarian drilling

236
Q

What is the success rate of intrauterine insemination per cycle?

A

10-20% per cycle.

237
Q

What is the rationale behind SC injections of FSH in the days leading up to intrauterine insemination?

A

It aims to stimulate the ovaries to produce 2-3 mature follicles (this process is known as stimulated IUI).

NOTE: Follicular tracking with ultrasound is essential to avoid over- or under-stimulation.

238
Q

When performing intrauterine insemination, how can we trigger ovulation and time the insemination?

A

SC hCG injection - this mimics the endogenous LH surge.

239
Q

How is pituitary dow-regulation achieved in IVF, and why?

A

A GnRH agonist is used to block FSH and LH release, in order to prevent endogenous LH surges and premature ovulation.

240
Q

How is controlled ovarian stimulation achieved in IVF, and why?

A

Daily SC doses of gonadotrophins are given in order to cause multiple follicle recruitment.

NOTE: Close monitoring with TVUSS predicts the numbers of follicles and the timing of the egg collection.

241
Q

In IVF, how long after the hCG trigger do we perform egg collection? How is egg collection performed?

A

Egg collection occurs 37 hours after the hCG trigger (which mimics the endogenous LH surge). Under anaesthesia, a needle is inserted into the ovaries under TVUSS control, and follicular fluid is aspirated from each follicle that contains an oocyte.

242
Q

What is it called when individual sperm are isolated and directly injected into the cytoplasm of an oocyte in IVF (this is done if the sperm are poor)?

A

Intracytoplasmic sperm injection (ICSI).

243
Q

What are the success rates of IVF and ICSI respectively?

A
IVF = 60%
ICSI = 70%
244
Q

How is the embryo usually transferred into the uterus following IVF?

A

Using a soft plastic catheter.

245
Q

What is meant by the term embryo cryopreservation with regards to IVF?

A

Spare embryos of good quality can be frozen and preserved for future use if the initial embryo implantation fails. These have the same success rate as fresh embryos.

246
Q

Why are patients undergoing IVF given supplementary progesterone following egg collection?

A

Because use of gonadotrophin agonists/antagonists to prevent premature lH surge causes a reduction in the corpus luteum’s ability to produce progesterone.

247
Q

How long after embryo transfer is a pregnancy test performed in IVF?

A

14 days.

248
Q

What is the main risk of IVF?

A

Ovarian hyperstimulation syndrome (OHSS).

249
Q

How does ovarian hyperstimulation syndrome present?

A

Ascites
Enlarged multifollicular ovaries
Pulmonary oedema
Coagulopathy

250
Q

Define menopause.

A

A woman’s final period. The accepted confirmation of this is made retrospectively after 1 year of amenorrhoea.

251
Q

Define perimenopause.

A

Time from the onset of ovarian dysfunction until 1 year after the last period.

252
Q

What is the median age of menopause?

A

51-52 years.

253
Q

Where is inhibin B produced?

A

The ovarian follicles - as the number of follicles declines, the production inhibin B declines.

254
Q

Why do FSH and LH levels rise during perimenopause?

A

Declines in inhibin (due to decline in number of follicles) drive an overalll increase in pulsatility of GnRH secretion and overall FSH and LH levels.

255
Q

Define premature ovarian insufficiency.

A

Menopause occurring before the age of 40 years.

256
Q

What are the primary (3) and secondary (2) causes of primary ovarian insufficiency?

A

Primary:
Chromosomal abnormalities (e.g. Turner’s syndrome)
Autoimmune disease
Enzyme deficiencies (e.g. galactosaemia)

Secondary:
Chemo/radiotherapy
Infections (e.g. TB)

257
Q

Which medications can cause a ‘temporary menopause’ and how?

A

GnRH agonists (used to treat endometriosis and other gynaecological issues) - constant stimulation of GnRH receptors leads to desensitisation and reduces LH and FSH release.

258
Q

Vasomotor symptoms of menopause (hot flushes/night sweats) are some of the earliest changes seen - why are they thought to occur?

A

Thought to be due to loss of the modulating effect of oestrogen on sertoninergic receptors within the thermoregulatory centre in the brain.

259
Q

What can trigger hot flushes in menopausal women? (3)

A

Alcohol
Caffeine
Smoking

260
Q

Why are menopausal/post-menopausal women at higher risk of UTIs?

A

The urogenital system becomes weaker as a barrier to infection due an increase in pH.

261
Q

Why do menopausal women get vaginal dryness, irritation, burning, soreness and dyspareunia?

A

Loss of oestrogen support of the vaginal epithelium leads to reduced cellular turnover and glandular activity. This makes the vaginal epithelium less elastic and more easily traumatised.

262
Q

Define osteoporosis. How much more common is it in women than in men?

A

A skeletal disorder characterised by compromised bone strength predisposing to an increased fracture risk. It is 4x more common in women.

263
Q

How does fat distribution change after menopause?

A

There is a change from a gynaecoid (breast and hip fat) to an android (abdominal fat) distribution.

264
Q

What changes to triglycerides and cholesterols occur at menopause?

A

Rise in triglycerides
Rise in total cholesterol
Rise in LDLs
Decline in HDLs

265
Q

What non-hormonal medical treatments can be offered to women going through menopause (offering symptomatic relief)? (3)

A

Alpha agonists (e.g. clonidine)
Beta-blockers (e.g. propranolol)
Modulators of central neurotransmission (e.g. venlafaxine, fluoxetine, citalopram, gabapentin)

NOTE: Other symptomatic treatments include vaginal moisturisers, lubricants and osteoporosis treatments (bisphosphonates, raloxifene etc.).

266
Q

Which progestogens are used in HRT? (6)

A
Norethisterone
Levonorgestrel
Dydrogesterone
Medroxyprogesterone acetate
Drospirenone
Micronised progesterone
267
Q

Why should oestrogens only be given without progestognenic opposition in HRT in women who have undergone hysterectomy?

A

Because oestrogens without progestognenic opposition carry a risk of endometrial hyperplasia and cancer - this is not an issue if the patient has no uterus.

268
Q

What does a cyclical HRT regimen usually look like?

A

28 days:
16-18 days = oestrogen alone
10-12 days = oestrogen and progesterone

NOTE: This results in monthly menstruation.

269
Q

Who qualifies for continuous combined HRT?

A

Women known to be post-menopausal or women 54+ years of age.

270
Q

What are the negatives of giving HRT orally?

A

It influences lipid metabolism and the coagulation system through its effect on the liver during first-pass metabolism.

271
Q

What are the absolute contraindications of HRT? (8)

A
Suspected pregnancy
Breast cancer
Endometrial cancer
Active liver disease
Uncontrolled hypertension
Known current VTE
Known thrombophilia
Otosclerosis
272
Q

What are the progestogen associated side-effects of HRT? (6)

A
Fluid retention
Breast tenderness
Headaches
Mood swings
Depression
Acne
273
Q

What are the oestrogen associated side-effects of HRT? (4)

A

Breast tenderness/swelling
Nausea
Leg cramps
Headaches

274
Q

What is the most common cause of abnormal vaginal discharge?

A

Bacterial vaginosis.

275
Q

What is thought to cause bacterial vaginosis (the definitive cause is not known)?

A

Depletion of lactobacilli in the healthy vaginal flora.

276
Q

Bacterial vaginosis (BV):
Risk factors (5)
Symptoms
Management

A
Risk factors:
Douching
Afro-Caribbean
Smoking
New sexual partner
Receiving oral sex

Symptoms - homogenous off-white vaginal discharge with high pH (> 4.5) and a ‘fishy’ odour.

Management:
Oral or intravaginal treatment with metronidazole or clindamycin.

277
Q

Vulvovaginal candidiasis diagnosis and management.

A

Diagnosis = bacterial swab for microscopy and culture.

Management:
Most women = intravaginal anti fungal cream or pessary (clotrimazole), or an oral antifungal (fluconazole).
Women > 60 years = oral antifungals due to ease of administration.
Girls aged 12-15 years = topical antifungal (avoid intravaginal or oral).
If vulval symptoms, give additional topical antifungal cream.

278
Q
Trichomoniasis:
Causative organism (and type of organism)
Route of transmission
Diagnosis
Management
A
Causative organism (and type of organism):
Trichomonas vaginalis (TV) - a flagellate protozoan.

Route of transmission = sexually transmitted.

Diagnosis = NAAT (nucleic acid amplification test) on vaginal or endocervical swab or urine.

Management = metronidazole.

279
Q

What are the possible causes of cervicitis and pelvic inflammatory disease (PID)? (2)

A

Gonorrhoea

Chlamydia

280
Q

How is gonorrhoea diagnosed and managed?

A
Diagnosis = NAAT
Management = ceftriaxone IM
281
Q

Reactive arthritis is a possible complication of which STI?

A

Chlamydia (RA is more common in men with chlamydia).

282
Q

Chlamydia diagnosis and management.

A
Diagnosis = NAAT
Management = Azithromycin or doxycycline
283
Q

Pelvic inflammatory disease (PID) signs and symptoms.

A
Lower abdominal pain
Dyspareunia
Altered vaginal discharge
Abnormal vaginal bleeding
Cervicitis
284
Q

Complications of pelvic inflammatory disease (PID). (4)

A

Subfertility - caused by endometrial and Fallopian tube inflammation and damage
Ectopic pregnancy
Chronic pelvic pain
Fitz-Hugh Curtis Syndrome - unusual complication where the patient experiences RUQ pain due to perihepatitis

285
Q

What is Fitz-Hugh Curtis syndrome?

A

An unusual complication of pelvic inflammatory disease (PID) where the patient experiences RUQ pain due to perihepatitis.

286
Q

Management of pelvic inflammatory disease (PID).

A

If an IUD is in situ, consider removal
Macrolide OR tetracycline AND metronidazole with a 3rd generation cephalosporin
Screen sexual partners and give empirical treatment with azithromycin

287
Q

What are the 2 types of genital herpes?

A

HSV1 (orolabial herpes)

HSV2 (genital herpes)

288
Q

HSV1 and HSV2 establish latency where?

A

In the local sensory ganglia.

289
Q

Genital herpes symptoms and diagnosis.

A

Symptoms:
Genital pain
Dysuria
Multiple superficial tender ulcers with regional lymphadenopathy

Diagnosis:
PCR following swab of genital lesions
Consider serology to establish primary vs non-primary

290
Q

What is the mortality rate of neonatal herpes?

A

30% mortality (and lifelong neurological morbidity in 70%).

291
Q

Management of genital herpes.

A

Aciclovir (or valaciclovir).

292
Q

Genital warts:
Causative organism and types
Management

A

Causative organism:
HPV - types 6 and 11 cause 90% of genital warts, and types 16 and 18 are sexually transmitted but cause anogenital dysplasia and cancer.

Management:
Ablation with liquid nitrogen (cryotherapy)
Surgery
Topical methods (podophyllotoxin-containing preparation, imiquimod)

293
Q

What is the name of the rare complication seen in infants born to mothers wit HPV infection?

A

Respiratory pappilomatosis.

294
Q

Syphilis causative organism and routes of transmission (2).

A

Causative organism = treponema pallidum.

Routes of transmission:
Direct contact with secretions from infective lesions
Transplacental passage of bacteria during pregnancy

295
Q

How does syphilis usually first present?

A

Painless chancre (indurated and serous fluid containing).

296
Q

How does secondary syphilis present?

NOTE: It typically resolves spontaneously as the immune response clears it.

A

Widespread erythematous rash including the palms and soles.

Can also result in alopecia, oral and genital mucous lesions and raised lesions in the anogenital area called condylomata lata.

297
Q

What are the complications of syphilis? (6)

A

Meningitis
8th nerve palsy leading to deafness/tinnitus
Ophthalmic involvement (uveitis)
Gummatous lesions
Cardiovascular disease (aortic valve incompetence)
Neurological involvement

298
Q

What are the common manifestations of congenital syphilis (presenting within 2 years of life)? (5)

NOTE: Syphilis is part of routine antenatal screening.

A
Rash
Skeletal abnormalities
Haemorrhagic rhinitis (bloody sniffles)
Generalised lymphadenopathy
Hepatosplenomegaly
299
Q

How is syphilis diagnosed?

A

Serology
Direct detection of T. pallidum via microscopy or PCR

Non-treponemal serological tests - rapid plasma reagin, venereal disease reference laboratory (VDRL).
Treponemal tests - enzyme immunoassay (EIA), chemiluminescence immunoassay (CLIA), treponema pallidum particle or haemagluttination assay (TPPA/TPHA).

300
Q

Management of syphilis.

A

Penicillin-based regimens (curative).

301
Q

Why is annual cervical cytology recommended in female patients with HIV?

A

Because there is higher incidence of cervical intraepithelial neoplasia (CIN) and high0grade squamous intraepithelial lesion (HSIL).

302
Q

What is meant by the term urge incontinence?

A

Involuntary leakage accompanied by or immediately preceded by urgency.

303
Q

What is meant by the term stress incontinence?

A

Involuntary leakage on effort, exertion, sneezing or coughing.

304
Q

Stress incontinence is suggestive of an incompetent urethral sphincter. What is the most common cause of this?

A

Hypermobility - the pelvic floor and ligaments cannot retain the urethra in position and it falls through the urogenital hiatus during increases in abdominal pressure. This leads to a loss of intra-abdominal pressure transmission to the urethra leading to leakage of urine.

305
Q

Causes of stress incontinence. (2)

A

Hypermobility

Intrinsic sphincter deficiency (ISD)

306
Q

What is detrusor overactivity?

A

Involuntary detrusor contractions during the filling phase of micturition - women will complain of symptoms of an overactive bladder but may not be incontinent unless urethral sphincter function is compromised.

307
Q

What investigations should be considered in a patient with urinary incontinence?

A

MSU
Bladder diary (usually 3 days)
Pad test
Pelvic or renal USS

308
Q

Why might reducing fluid intake result in an increased sensation of urgency?

A

Due to more concentrated urine.

309
Q

What are the elements of conservative management of urinary incontinence? (4)

A

Advice about fluid balance - 1.5-2.5 litres of water per day.
Reduction in caffeine intake.
Bladder retraining.
Pelvic floor muscle exercises.

310
Q

How does urodynamic testing work (to assess urinary incontinence)?

A

A fine pressure catheter is placed in the bladder, and a second is inserted into the rectum. The bladder is filled with warm saline whilst pressure recordings are made with the patient sitting on a commode that records leakage. The patient reports on sensations of desire to void and urgency.

311
Q

Why are anticholinergic medications the mainstay of medical treatment for urinary incontinence?

A

Because parasympathetic nerve stimulate the detrusor muscle to contract.

312
Q

Give some examples of anticholinergic medications used to treat urinary incontinence, identifying the NICE recommended medication.

A
Oxybutynin - NICE recommended
Propiverine
Trospium
Tolterodine
Fesoterodine
Solifenacin
Darifenacin
313
Q

What is mirabegron and what can it be used to treat?

A

A new beta-3 adrenergic agonist that enhances detrusor relaxation - it can be used to treat overactive bladder.

314
Q

What are the best surgical options for treatment of stress incontinence (2), and what are the complications (4)?

A

Synthetic midurethral tape procedure
Burch colposuspension

Complications:
Voiding difficulty (both)
Bladder perforation during procedure (both)
Onset of new OAB symptoms after surgery (both)
Posterior vaginal prolapse (Burch colposuspension)

NOTE: These both have a cure rate of 80-85%.

315
Q

What surgical procedure can be used to treat stress incontinence in women deemed unfit for general anaesthesia?

A

Periurethral injections to bulk up the bladder neck and coat the urethral mucosa.

316
Q

How can we surgically manage detrusor overactivity?

A

Botulinum toxin injections to precent involuntary detrusor contractions.

317
Q

What are the 3 levator ani muscles?

A

Puborectalis
Pubococcygeus
Iliococcygeus

318
Q

What is the urogenital hiatus?

A

A gap in the puborectalis to allow the passage of the urethra, vagina and rectum.

319
Q

What are the 3 levels of supporting ligaments and fascia which support the uterus, vagina and other organs?

A

Level 1 - Apical:
Uterosacral ligaments attach the cervix to the sacrum
Defects in level 1 can lead to descent of the uterus within the vagina

Level 2:
Fascia around the vagina or rectovaginally - the fascial sheets fuse at the vaginal edge and are attached to the pelvic side wall
Defects in level 2 result in prolapse of the vaginal wall into the vaginal lumen

Level 3:
Fascia of the posterior vagina (attached to the caudal end of the perineal body)
Defects of the perineal body cause development of lower posterior vaginal wall collapse

320
Q

What are the 3 stages of descent with regards to prolapse?

A

Stage 1 = prolapse does not reach the hymen
Stage 2 = prolapse reaches the hymen
Stage 3 = prolapse is mostly or wholly outside the hymen

321
Q

What is it called when the uterus prolapses wholly outside the hymen?

A

Procidentia.

322
Q

What is vaginal prolapse of the anterior vagina called?

A

Cystocele - in the upper half of the vagina

Urethrocele - in the lower half of the vagina

323
Q

What is vaginal prolapse of the posterior vagina called?

A

Enterocele - in the upper third of the vagina

Rectocele - in the lower 2/3 of the vagina

324
Q

What are the aspects of conservative treatment of uterovaginal prolapse? (2)

A

Pelvic floor exercises

Supportive vaginal pessaries

325
Q

Ovarian torsion:
Definition
Diagnosis
Management

A

Definition - rotations of the vascular pedicle supplying the ovary, which compresses and cuts its blood supply.

Diagnosis - pelvic USS with Doppler measurement of blood flow.

Management - surgery to untwist ovary/pedicle, and remove any ovarian cysts.

326
Q

What are the tumour markers to check in patients with ovarian cysts, and which cancers do they relate to? (5)

A

Ca 125 - epithelial ovarian cancer (serous)
Ca 19-9 - epithelial ovarian cancer (mucinous)
Inhibin - granulosa cell tumours
Beta-hCG - dysgerminoma, choriocarcinoma
AFP - endodermal yolk sac, immature teratoma

327
Q

What are the 3 types of functional ovarian cyst?

A

Follicular cyst
Corpus luteal cyst
Theca lutein cyst

328
Q

What is the relationship between the COCP and functional ovarian cysts?

A

COCP reduces the risk of functional ovarian cysts.

329
Q

When do corpus luteal cysts occur?

A

Following ovulation - they may present with pain due to rupture or haemorrhage.

330
Q

When do theca lutein cysts occur?

NOTE: They are often bilateral.

A

Usually during pregnancy.

331
Q

What are endometriomas? What is their characteristic appearance on USS?

A

When endometrial tissue is implanted into an ovary, an endometrioma forms. These are known as ‘chocolate cysts’ due to the presence of altered blood within the ovary.

USS = ground glass appearance.

332
Q

What is the most common form of benign germ cell tumour?

A

Mature dermoid cyst (cystic teratoma) - contains fully differentiated tissue types from all 3 germ cell layers.

333
Q

Ovarian epithelial tumours are most commonly seen in women of what age?

A

Perimenopausal women (late 40s, early 50s).

334
Q

What is the most common type of ovarian epithelial tumour?

A

Serous cystadenoma.

335
Q

How can you (often) differentiate a serous cystadenoma from a mucinous cystadenoma?

A
Serous = unilocular and unilateral
Mucinous = multilocular and bilateral
336
Q

What are Brenner tumours?

A

Small tumours usually found incidentally in the ovaries, which contain urothelial-like epithelium and may (rarely) secrete oestrogen.

337
Q

What is the most common type of sex cord stromal tumour?

A

Ovarian fibroma - solid ovarian tumour composed of stromal cells.

338
Q

How do sex cord stromal tumours tend to present?

A

With ovarian torsion.

339
Q

What is Meig syndrome?

A

Pleural effusion, ascites and ovarian fibroma.

340
Q

What is a thecoma?

A

A benign oestrogen0secreting tumour that tends to present after menopause and can induce an endometrial carcinoma.

341
Q

What is endometriosis and where is it commonly found?

A

Endometrial tissue lying outside the uterine cavity - it is commonly found on the peritoneum lining the pelvic side walls, pouch of Douglas, uterosacral ligaments and bladder.

342
Q

Adenomyosis is often associated with endometriosis. What is adenomyosis?

A

A disorder in which endometrial glands and stroma are found deep within the myometrium.

343
Q

Why does endometriosis resolve after menopause?

A

Because it is oestrogen-dependent.

344
Q

Which 2 theories exist to explain the aetiology of endometriosis?

A

Sampson’s Implantation theory - retrograde menstrual regurgitation of viable endometrial glands along patent Fallopian tubes and subsequent implantation on the pelvic peritoneal surface causes endometriosis.

Meyer’s Coelomic Metaplasia theory - Coelomic epithelium transformation refers to the de-differentiation of peritoneal cells lining the Mullerian duct back to their primitive origin (which then become endometrial cells).

345
Q

What are the general symptoms of endometriosis (ignore site-specific symptoms)?

A

Severe cyclical non-colicky pelvic pain (occurs around time of menstruation)
Heavy menstrual bleeding
Severe fatigue

346
Q

What are the key indicators of the presence of endometriosis deep within the pouch of Douglas?

A

Deep dyspareunia

Dyschezia (pain on defecation)

347
Q

Which findings on physical examination may indicate endometriosis? (4)

A

Thickening or nodularity of the uterosacral ligaments
Tenderness in the pouch of Douglas
Adnexal mass
Fixed retroverted uterus

348
Q

What proportion of patients with endometriosis complain of difficulty conceiving?

A

30-40%. Medical treatment has no effect on this but surgical treatment can improve fertility.

349
Q

Why should opiates be avoided in the analgesic treatment of endometriosis?

A

They could worsen co-existing IBS.

350
Q

What are the medical treatment options for endometriosis? (4)

A

Analgesia - NSAIDs
COCP
Progestogens
GnRH agonists

351
Q

What are the surgical options for the treatment of endometriosis? (2)

A

Fertility-sparing surgery (ablation/excision of superficial endometriosis deposits)
Hysterectomy and oophorectomy

352
Q

Define chronic pelvic pain.

A

Intermittent or constant pain in the lower abdomen or pelvis of a woman of at least 6 months duration, not occurring exclusively with menstruation or intercourse and not associated with pregnancy.

353
Q

What is cervical ectropion?

A

A condition in women of reproductive age, where the columnar epithelial is visible on the ectocervix as a road, red area surrounding the external cervical os (this is NORMAL).

354
Q

Cervical ectropion normally develops under the influence of the 3 Ps - what are they?

A

Puberty
Pill
Pregnancy

355
Q

When might cervical ectropion be considered a problem and how can it be managed?

A

It can become a problem as large ectropion may be fragile leading to intermenstrual and post-coital bleeding. Some women also complain of excessive, clear, odourless, mucous-type discharge.

Management:
Cervical ablation
Changing from oestrogen-based hormonal contraceptives

356
Q

What are Nabothian follicles?

A

Small, mucous-filled cysts visible on the ectocervix when the columnar glands within the transformation zone become sealed over. They are not clinically significant.

357
Q

What are cervical polyps? How can they be treated and when would you consider treatment?

A

They are benign tumours arising from the endocervical epithelium.

They can cause vaginal discharge, intermenstrual bleeding and post-coital bleeding. Easily removed by avulsion with polyp forceps as an outpatient.

358
Q

Cervical stenosis:
What is it?
What causes it?
How is it managed?

A

What is it?
Pathological narrowing of the endocervical canal.

What causes it?
Often iatrogenic (cone biopsy, loop diathermy and endometrial ablation).

How is it managed?
Surgical dilatation of the cervix under ultrasound or hysteroscopic guidance.

359
Q
Endometrial polyps:
What are they?
Risk factors (4)
Investigations (2)
Management
A

What are they?
Focal endometrial outgrowths containing a variable amount of glands, stroma and blood vessels (so varying in appearance). They can cause abnormal uterine bleeding and fertility issues.

Risk factors:
Obesity
Late menopause
Tamoxifen
HRT

Investigations:
TVUSS
Outpatient hysteroscopy and saline infusion sonography

Management:
May resolve spontaneously
Polypectomy

360
Q

Asherman Syndrome:
Definition
Causes (3)
Management

A

Definition - fibrosis and adhesion formation within the endometrial cavity following irreversible damage of the single layer thick basal endometrium.

Causes:
After pregnancy that was complicated by uterine infection (endometritis)
After overzealous curettage of the uterine cavity during surgical management of miscarriage
After surgical management of postpartum haemorrhage

Management:
Surgical adhesiolysis

361
Q

What are the three forms of degeneration of fibroids (due to outgrowing their blood supply)?

A

Red - haemorrhage and necrosis occurs within the fibroid (typically presenting mid-second trimester of pregnancy with acute pain).

Hyaline - asymptomatic softening and liquefaction of the fibroid.

Cystic - asymptomatic central necrosis leaving cystic spaces at the centre - can lead to calcification or malignant degeneration.

362
Q

What is the only effective medical treatment for fibroids?

A

Injectable GnRH agonists - poorly tolerated because of severe menopausal symptoms.

NOTE: Ulipristal acetate (selective progesterone receptor modulator) is as effective and does not induce a menopausal state, but is not yet used clinically.

363
Q

Uterine artery embolisation (UAE) can be used to treat fibroids (causes infarctions and reduction in volume of around 50%) - what are the complications? (4)

A

Fever
Infection
Fibroid expulsion
Ovarian failure

364
Q

What is the only definitive method of diagnosing adenomyosis?

A

Histopathological examination of a hysterectomy specimen. MRI is the best investigation otherwise.

365
Q

Clinical manifestation of adenomyosis.

A

Increasingly severe secondary dysmenorrhoea
Uterine enlargement
Heavy menstrual bleeding

366
Q

Management of adenomyosis.

A

Any treatment that induces amenorrhoea with relieve symptoms - consider progestin-containing long-acting reversible contraceptives (LNG-IUS, DepoProvero etc.).

Hysterectomy is the only definitive treatment.

367
Q

What are the types of ovarian cancer?

A
Epithelial:
High grade serous
Endometroid
Clear cell
Mucinous
Low-grade serous

Sex Cord Stromal:
Granulosa cell
Sertoli-Leydig
Gynandroblastoma

Germ Cell:
Dysgerminoma
Endodermal sunus (yolk sac)
Teratoma
Choriocarcinoma
Mixed

Secondary ovarian cancers (Krukenberg tumour)

368
Q

What are borderline ovarian tumours (BOTs)?

A

Well-differentiated tumours with some features of malignancy, that do not invade the basement membrane.

369
Q

What proportion of all epithelial ovarian cancers are high-grade serous carcinomas?

A

75%

370
Q

High-grade serous carcinoma is characterised by what?

A

Psammoma bodies (concentric rings of calcification).

371
Q

Which ovarian cancers are associated with pseudomyxoma peritoneii?

A

Mucinous carcinomas (a form of epithelial ovarian cancer).

372
Q

Which 2 forms of epithelial ovarian cancer can arise from endometriosis?

A

Endometrioid carcinoma

Clear cell carcinoma

373
Q

What is serous tubal intraepithelial carcinoma (STIC)?

A

A precursor lesion to high-grade pelvic serous carcinoma, found in the Fallopian tubes and characterised by p53 mutations in secretory cells of the distal Fallopian tube.

374
Q

What proportion of high-grade pelvic serous carcinomas have BRCA mutations?

A

30%

375
Q

Increased risk of ovarian cancer is associated with BRCA1 and BRCA2, as well as which genetic syndrome?

A

Lynch syndrome (HNPCC) - this is associated with endometrial cancer.

376
Q

What can we do to prevent ovarian cancer? (3)

A

Offer bilateral salpingo-oophorectomy (BSO) to BRCA positive women who have completed their families
Tubal ligation and hysterectomy
COCP

377
Q

Ca125 is a tumour marker associated with epithelial ovarian cancer and (serous) borderline ovarian tumours. It is also commonly raised in which 3 conditions?

A

Pregnancy
Endometriosis
Alcoholic liver disease

378
Q

What is risk of malignancy index (RMI)?

A

An index that uses menopausal status, pelvic ultrasound features and Ca125 to triage pelvic masses, assessing risk of ovarian cancer. If there is high risk, follow up with CT/MRI.

379
Q

How is ovarian cancer staged?

A

FIGO staging - staged 1, 1a, 1b, 1c, 2 etc. up until 4.

1 = tumour confined to ovaries.
4 = distant metastases with positive cytology on pleural effusion or liver parenchyma.
380
Q

What is ‘second look’ surgery with regards to ovarian cancer?

A

Planned laparotomy at the end of chemotherapy - this aims to assess residual disease.

381
Q

What is the first line chemotherapy regimen for patients with ovarian cancer?

A

Combination of a platinum compound with paclitaxel (usually given as an outpatient, 3 weeks apart for 6 cycles).

382
Q

Carboplatin (for ovarian cancer):
How does it work?
Why do we use it over cisplatin?
How do we calculate dose?

A

How does it work?
Causes cross-linkage of DNA strands leading to cell cycle arrest.

Why do we use it over cisplatin?
It is less nephrotoxic and causes less nausea.

How do we calculate dose?
Using the GFR.

383
Q

Why are pre-emptive steroids given to patients before they receive paclitaxel?

A

To reduce hypersensitivity reactions and side-effects such as peripheral neuropathy, neutropenia and myalgia.

384
Q

Bevacizumab is not routinely used to treat ovarian cancer due to the cost, but can be used to treat recurrent disease. How does it work?

A

It is a monoclonal antibody against VEGF which inhibits angiogenesis.

385
Q

Primary peritoneal carcinoma (high-grade serous carcinoma) diagnostic criteria. (3)

A

Normal sized or slightly bulky ovaries
More extra ovarian disease than ovarian disease
Low volume peritoneal disease

386
Q

Sex cord stromal tumours are common but do not often undergo malignant transformation. Morbidity tends to arise from oestrogen or androgen production. What is the most common type of sex cord storm tumour?

A

Granulosa cell tumour.

387
Q

Why might Sertoli-Leydig cell tumours cause hypertension?

A

They can be renin-producing.

388
Q

What are the first and second most common types of germ cell tumour?

A
Dysgerminoma
Endodermal sinus (yolk sac) tumour
389
Q

Which tumour marker is secreted by yolk sac tumours?

A

AFP

390
Q

What is the most common chemotherapy regime given to patients with germ cell tumours?

A

Bleomycin, etoposide and cisplatin (BEP) - given as 3-4 treatments 3 weeks apart. Has a 90% cure rate.

391
Q

What is the most common gynaecological malignancy?

A

Endometrial cancer.

392
Q

How is endometrial cancer classified?

A

Type 1 - endometriosis carcinomas:

  • Oestrogen driven
  • Arise from background of endometrial hyperplasia

Type 2 - high-grade serous or clear cell carcinomas:
- Arise from atrophic endometrium

These cancers are then graded 1-3 (3 = high-grade).

393
Q

How can we prevent endometrial cancer in patients with Lynch syndrome?

A

Offer prophylactic hysterectomy following completion of family.

394
Q

What is the red flag symptom of endometrial cancer?

A

Post-menopausal bleeding.

395
Q

How can TVUSS be used to assess likelihood of endometrial cancer?

A

Allows assessment of endometrial thickness:
< 4mm = unlikely
> 4mm = requires further evaluation by hysteroscopy and/or biopsy

396
Q

What is complex hyperplasia with atypia?

A

A premalignant condition that often co-exists with low-grade endometrioid tumours of the endometrium.

397
Q

How is endometrial cancer staged (following MRI)?

A

FIGO staging - I to IV.

I = confined to uterine body.
IV = tumour invades bladder +/- bowel +/- distant metastases.
398
Q

What is the standard surgery for endometrial cancer?

A

Total hysterectomy with bilateral salpingo-oophorectomy.

399
Q

Which hormonal treatment can be used in patients with complex hyperplasia with atypia and low-grade stage 1A endometrial tumours?

A

High-dose oral or intrauterine progestins.

400
Q

What are the types of pure endometrial sarcoma? (2)

A

Endometrial stromal sarcoma

Leiomyosarcoma

401
Q

What are heterologous sarcomas and what is the most common type?

A

Heterologous sarcomas are uterine cancers consisting of sarcomatous tissue not usually found in the uterus (e.g. striated muscle, bone and cartilage).

Most common type = rhabdomyosarcoma.

402
Q

Which 2 types of HPV are associated with high risk of cervical cancer?

A

16 and 18.

403
Q

The transformation zone (TZ) is the site where cervical malignancy and pre-malignancy develop - where is it?

A

It is the area between the original squamocolumnar junction and the current one, where the epithelium changes from columnar to squamous over time.

(there is an original SCJ and a current SCJ because its position changes throughout life - in children is lies in the external cervical os, at puberty is extends outwards to the ectocervix and in adulthood is returns to the external cervical os)

404
Q

What are the features of immature cells seen in cervical intraepithelial neoplasia (CIN)? (4)

NOTE: CIN can be classified as CIN1 - CIN3 (3 = high grade).

A

Hyperchromatic
Large nuclei
Minimal cytoplasm
Abnormal mitotic features

405
Q

What is liquid-based cytology (LBC)?

A

A technique by which a small brush is used to sample cells from the transition zone of the cervix and the brush is placed in a fixative.

406
Q

What is dyskaryosis?

A

Abnormal cervical cytology showing squamous cells at different stages of maturity.

407
Q

The National Cervical Screening Programme offers screening to female patients aged ______ years old, every _____ years.

A

The National Cervical Screening Programme offers screening to female patients aged 25-64 years old, every 3-5 years.

408
Q

Colposcopy:
What is it?
What are acetic acid and iodine solutions used for?

A

What is it?
Examination of the magnified cervix using a light source.

What are acetic acid and iodine solutions used for?
Acetic acid - makes areas of increased cell turnover (including CIN) turn white.
Iodine - areas of CIN lake intracytoplasmic glycogen, so they fail to stain brown with iodine.

409
Q

How long after initial diagnosis should low-grade CIN be followed up with colposcopy and cytology?

A

6 months.

410
Q

High-grade CIN can be treated with various forms of excision or ablation - what is the favoured method?

A

Large Loop Excision of the Transformation Zone (LLETZ) - loop diathermy which only takes 15 minutes under local anaesthetic.

411
Q

What are the risks of large loop excision of the transformation zone (LLETZ)? (2)

A

Increased risk of mid-trimester miscarriage

Increased risk of preterm delivery

412
Q

The HPV vaccination programme provides vaccines to school girls aged _____ years, and protects against which types of HPV?

A

Given to school girls aged 12-13 years and protects against types 6, 13, 16 and 18.

413
Q

Why might advanced cervical cancer cause renal failure?

A

Due to ureteric blockage.

414
Q

Squamous cell carcinomas make up what proportion of cervical cancers?

A

70% (the rest are adenocarcinomas).

415
Q

What is cervical glandular intraepithelial neoplasia (CGIN)?

A

A precursor to cervical adenoma which can be detected on colposcopy.

416
Q

How is cervical cancer staged?

A

FIGO staging - I to IV.

I = confined to cervix.
IVB = spread to distant organs.
417
Q

Preclinical cervical lesions (stage 1A) can be removed with a clear margin. What is the management for clinically invasive cervical carcinoma (stages 1B-4)?

A

If small volume disease confined to the cervix:
Radical hysterectomy and bilateral pelvic node dissection (Wertheim’s hysterectomy).
If fertility sparing is required, radical trachelectomy and pelvic node dissection.

If beyond cervix, radiotherapy is the mainstay of treatment:
External beam radiotherapy
Internal radiotherapy (brachytherapy)

Chemotherapy:
Usually cisplatin

418
Q

What are the risks associated with radical hysterectomy and bilateral pelvic node dissection (Wertheim’s hysterectomy)? (3)

NOTE: This is used to treat cervical cancers confined to the cervix.

A
Bladder dysfunction (atony)
Sexual dysfunction (due to vaginal shortening)
Lymphoedema (due to pelvic lymph node removal)
419
Q

What proportion of vulval malignancies are squamous cell carcinoma?

A

90% (remainder are malignant melanoma, BCC and adenocarcinoma of the Bartholin’s gland).

420
Q

What are the 2 types of squamous cell carcinoma of the vulva?

A

High-risk HPV associated - usually in young women, arising on a background of high-grade vulval intraepithelial neoplasia (VIN3).

Non-HPV associated - usually in older women, associated with lichen sclerosus.

421
Q

How do vulval cancers spread?

A

They spread locally and metastasise via the inguinofemoral lymph nodes before the pelvic nodes.

422
Q

Management of vulval cancer.

A

Vulval excision (aim for 10mm margin)
Sentinel lymph node biopsy (likely followed by full inguinofemoral lymphadenectomy for all tumours with depth of invasion > 1mm)
Radiotherapy

423
Q

What are the main vessels supplying the uterus and adnexae?

A

The ovarian vessels (arising fro the aorta and renal artery) and the uterine vessels (branches of the posterior trunk of the internal iliac artery which run medially to the broad ligament).

424
Q

The ureter runs from the kidney over the _____ muscle and enters the pelvis where?

A

The ureter runs from the kidney over the psoas muscle and enters the pelvis over the sacroiliac joint.

425
Q

Which 3 pedicles need to be removed in hysterectomy?

A

Infundibulopelvic ligament (containing ovarian vessels)
Uterine artery
Angles of the vault of the vagina (containing vessels ascending from the vagina)

426
Q

What are the 2 types of hysterectomy?

A

Abdominal and vaginal.

427
Q

Where is a pfannenstiel incision? What incision can be made if extension of a pfannenstiel is required?

A

Where is a pfannenstiel incision?
Transversely, two finger breadths above the pubic symphysis.

What incision can be made if extension of a pfannenstiel is required?
Inverted T incision.

428
Q

Where is a midline incision?

A

Vertically from the pubic symphysis up to the umbilicus.

429
Q

What are the possible complications of hysterectomy? (3)

A
Perforation of the uterus
Cervical damage (if dilatation is needed)
Ascending infection (if infection is present)
430
Q

What are the possible complications of laparoscopy (uncommon)? (2)

A

Damage to bowel/major blood vessels

Incisional hernia

431
Q

What are the possible complications of cystoscopy? (2)

A
UTI
Bladder perforation (very rare)