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Final Year > Obstetrics and Gynaecology > Flashcards

Obstetrics and Gynaecology Flashcards

1
Q

Outline the Hypothalamic-Pituitary-Gonadal Axis (HPGA)

A

Hypothalamus releases gonadotrophin-releasing hormone (GnRH)
GnRH stimulates anterior pituitary to produce LH and FSH
LH and FSH stimulate development of follicles in ovaries
Theca granulosa cells around follicles secrete oestrogen
Oestrogen has negative feedback effect on hypothalamus and anterior pituitary to suppress release of GnRH, LH and FSH

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2
Q

What is produced by the anterior pituitary?

A

LH and FSH

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3
Q

Outline oestrogen

A

Steroid sex hormone produced by ovaries in response to LH and FSH
17-beta oestradiol- Acts on tissues with oestrogen receptors to promote female secondary sexual characteristics

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4
Q

What does oestrogen stimulate?

A

Breast tissue development
Growth and development of female sex organs (vulva, vagina and uterus) at puberty
Blood vessel development in uterus
Development of endometrium

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5
Q

Outline progesterone

A

Steroid sex hormone produced by corpus luteum after ovulation
In pregnancy- Progesterone produced mainly by placenta from 10wks
Acts on tissues previously stimulated by oestrogen

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6
Q

Outline role of progesterone

A

Thicken and maintain endometrium
Thicken cervical mucus
Increase body temperature

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7
Q

Outline hormonal changes during pregnancy

A

GH increases initially- Growth spurt
Hypothalamus starts to secrete GnRH- Initially during sleep
GnRH stimulates release of FSH and LH from pituitary gland
FSH and LH stimulate ovaries to produce oestrogen and progesterone
FSH levels plateau a yr before menarche
LH levels continue to rise and spike just before induce menarche

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8
Q

What age do boys and girls start puberty?

A

Girls- 8-14y
Boys- 9-15y
Overweight children tend to enter puberty earlier- Aromatase is enzyme in adipose tissue- Important in creation of oestrogen
Before puberty girls have little GnRH/LH/FSH/oestrogen/progesterone

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9
Q

List causes of delayed puberty in girls

A

Low birth weight
Chronic disease
Eating disorders
Athletes

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10
Q

Outline Tanner staging

A

Stage I- <10y- No pubic hair- No breast development
Stage II- 10-11y- Light and thin PH- Breast buds from behind areola
Stage III- 11-13y- Course and curly PH- Breast begins to elevate beyond areola
Stage IV- 13-14y- Adult-like PH but not reaching thigh- Areolar mound forms and projects from surrounding breast
Stage V- >14y- PH extending to medial thigh- Areolar mounds reduce and adult breasts form

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11
Q

Outline the follicular phase of menstruation

A

Start of menstruation to moment of ovulation (0-14d of cycle)

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12
Q

Outline luteal phase of menstrual cycle

A

Moment of ovulation to start of menstruation (14-28d)

After ovulation, follicle that released ovum collapses and becomes corpus luteum
Corpus luteum secretes progesterone and maintains endometrial lining- Becomes thick and no longer penetrable- Also secretes small amount of oestrogen

In fertilisation- Syncytiotrophoblast of embryo secretes hCG- Maintains corpus luteum

No fertilisation- No hCG- Corpus luteum degenerates and stops producing oestrogen and progesterone- Fall in oestrogen and progesterone causes endometrium to breakdown and menstruation
Stromal cells of endometrium release prostaglandins- Encourage endometrium to breakdown and uterus to contract
Negative feedback from oestrogen and progesterone on hypothalamus and pituitary gland ceases- Allows level of LH and FSH to begin to rise and cycle restart

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13
Q

Outline formation of follicles

A

Oocytes surrounded by granulosa cells, forming follicles
1. Primordial follicles
2. Primary follicles
3. Secondary follicles- Requires FSH stimulation to develop into antral follicle
4. Antral follicles (Graafian follicles)

As follicles grow- Granulosa cells secrete increasing amounts of oestradiol- Negative feedback effect on pituitary gland, reducing quantity of LH and FSH
Rising oestrogen causes cervical mucus to become more permeable- Allows sperm to penetrate cervix around time of ovulation
One follicle develops more than other and becomes dominant
LH spikes just before ovulation, causing dominant follicle to release ovum from ovary

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14
Q

What is menstruation?

A

Superficial and middle layers of endometrium separating from basal layer
Tissue broken down inside uterus, and released via cervix and vagina
Release of fluid containing blood from vagina lasts 1-8d

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15
Q

Outline development of primary follicle

A

Primordial follicles grow and become primary follicles
Primary follicles have 3 layers:
1. Primary oocyte in centre
2. Zona pellucida
3. Cuboidal shaped granulosa cells

Granulosa cells secrete material that become zona pellucida- Secrete oestrogen
Follicles grow larger and develop surrounding layer called theca folliculi
- Inner layer- Theca interna- Secretes androgen hormones
- Outer layer- Theca externa- Made of connective tissue containing smooth muscle and collagen

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16
Q

Outline development of secondary follicle

A

Primary follicle grows larger and develop small fluid-filled gaps between granulosa cells
Develop receptors for FSH
Further development after secondary follicle stage requires stimulation from FSH
At start of menstrual cycle, FSH stimulates further development of secondary follicles

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17
Q

Outline development of antral follicles

A

Secondary follicle develops single large fluid-filled area within granulosa cells- Antrum- Antral follicle stage
Antrum fills with increasing fluid- Follicle expands rapidly
Corona radiata- Made of granulosa cells- Surrounds zona pellucida and oocyte
One of the follicles becomes dominant follicle and matures, bulging through wall of the ovary- Others degrade

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18
Q

Outline ovulation

A

Surge of LH from pituitary
Causes smooth muscle of theca externa to squeeze and follicle bursts
Follicular cells release digestive enzymes that puncture hole in wall of ovary- Ovum passes and escapes
Oocyte released into surrounding area and swept up by fimbriae of fallopian tubes

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19
Q

Outline corpus luteum

A

Leftover parts of follicle collapse and turn yellow
Collapsed follicle becomes corpus luteum
Cells of granulosa and theca interna become luteal cells
Luteal cells secrete steroid hormones- Progesterone
Corpus luteum persists in response to hCG from a fertilised blastocyst when pregnant
If fertilisation doesn’t occur- Corpus luteum degenerates after 10-14d

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20
Q

Outline fertilisation

A

Just before time of ovulation- Primary oocyte undergoes meiosis- Splits 46 chromosomes in oocyte in 2
Secondary oocyte has 23 chromosomes
Oocyte surrounded by zona pellucida surrounded by corona radiata (granulosa cells)
Sperm enters fallopian tube and attempts to penetrate corona radiata and zona pellucida to fertilise egg

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21
Q

Outline development of blastocyst

A

Combination of chromosomes from egg and sperm- Zygote
Cell divides rapidly to create mass of cells- Morula- Mass of cells travels along fallopian tube toward uterus
Fluid-filled cavity gathers within group of cells- Blastocyst
Blastocyst contains embryoblast and blastocele surrounded by trophoblast
Gradually loses corona radiata and zona pellucida
Enters uterus

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22
Q

Outline implantation of blastocyst

A

Arrives at uterus 8-10d after ovulation and reaches endometrium
Cells of trophoblast undergo adhesion to stroma of endometrium
Outer layer of trophoblast= Syncytiotrophoblast- Produces hCG
Cells of stroma convert into decidua- Provides nutrients to trophoblast
hCG maintains corpus luteum and produces progesterone and oestrogen

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23
Q

Outline development of embryo

A

Week after fertilisation- Implanted blastocyst differentiates
Cells of embryoblast splits in 2- Yolk sac and amniotic cavity
Cells of embryonic disc develop into fetal pole, then fetus
Chorion surrounds complex- 2 layers- Cytotrophoblast and syncytiotrophoblast
Chorionic cavity forms around yolk sac, embryonic disc and amniotic sac
Suspended from chorion by connecting stalk- Eventually becomes umbilical cord

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24
Q

What occurs in the fetus at 5wks?

A

Embryonic disc develops into fetal pole
Contains 3 layers- Ectoderm, mesoderm and endoderm

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25
Q

What occurs in the fetus at 6wks gestation?

A

Fetal heart forms and starts to beat
Spinal cord and muscles develop
Embryo (fetal pole) is about 4mm length

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26
Q

What does the endoderm become?

A

GI tract
Lungs
Liver
Pancreas
Thyroid
Reproductive system

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27
Q

What does the mesoderm become?

A

Heart
Muscle
Bone
Connective tissue
Blood
Kidneys

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28
Q

What does the ectoderm become?

A

Skin
Hair
Nails
Teeth
CNS

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29
Q

Outline development of the placenta

A

In follicular phase, endometrium thickens
Myometrium sends off artery branches into endometrium- Spiral arteries
Syncytiotrophoblast grows into endometrium and forms finger-like projections- Chorionic villi (contain fetal blood vessels)
Complete by 10wks gestation

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30
Q

Outline development of lacunae

A

Trophoblast invasion of endometrium sends signals to spiral arteries, reducing their vascular resistance- More fragile
Breakdown into lacunae (lakes)
Maternal blood flows from uterine arteries into lacunae and back out through uterine veins
Lacunae form at 20wks gestation
Lacunae surround chorionic villi, separated by placental membrane- Oxygen, CO2 and other substances diffuse across between mother and fetal blood

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31
Q

Outline the association between lacunae formation and pre-eclampsia

A

If process of forming lacunae inadequate- Can develop pre-eclampsia
Pre-eclampsia caused by high vascular resistance in spiral arteries
Sharp rise in maternal BP

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32
Q

Outline the role of the placenta in respiration

A

Source of oxygen for fetus
Fetal Hb has higher affinity for oxygen than adult Hb
Oxygen drawn off maternal Hb to fetal Hb
CO2, H+, HCO3-, and lactic acid also exchanged across placenta- Maintains acid-base balance

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33
Q

Outline role of placenta in nutrition

A

All nutrition comes from mother
Mostly in form of glucose- Energy and growth
Transfers vitamins and minerals to fetus

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34
Q

Outline role of placenta in excretion

A

Performs similar function to kidneys- Filters waste products from fetus
Eg: Urea and creatinine

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35
Q

Outline the endocrine function of the placenta

A

hCG- Levels increase in early pregnancy, plateau at 10wks gestation, then start to fall- Maintains corpus luteum until placenta takes over production of oestrogen and progesterone- Can cause nausea and vomiting

Oestrogen- Placenta produces oestrogen- Softens tissue and makes them more flexible- Allows muscles and ligaments of uterus and pelvis to expand- Cervix becomes soft and ready for birth- Enlarges and prepares breasts and nipples for breastfeeding

Progesterone- Placenta mostly takes over production by 5wks gestation- Maintains pregnancy- Causes relaxation of uterine muscles (prevents contraction and labour) and maintains endometrium

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36
Q

List some side effects of increased progesterone in pregnancy

A

Relaxes muscles:
- Lower oesophageal sphincter (heartburn)
- Bowel (constipation
- Blood vessels (hypotension, headaches and skin flushing)

Raises body temperature by 0.5-1 degrees C

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37
Q

What can cause increased levels of hCG, above that of normal pregnancy?

A

Multiple pregnancy (twins)
Molar pregnancy

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38
Q

Outline the role of the placenta in immunity

A

Mother’s antibodies transfer across placenta to fetus during pregnancy

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39
Q

What hormonal changes occur in pregnancy?

A

Raised:
Steroid hormones (cortisol and aldosterone)- Improves AI conditions but increases susceptibility to diabetes and infections
T3/T4 (TSH normal)
Prolactin- Suppresses FSH and LH
Melanocyte S.H.
Oestrogen- Rises throughout pregnncy, produced by placenta
Progesterone- Rise throughout pregnancy- Maintains pregnancy/prevents contractions/suppresses mother’s immune reaction to fetal antigen- Corpus luteum till 10wks, then placenta
hCG

Anterior pituitary produces more ACTH, prolactin and melanocyte stimulating hormone

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40
Q

What cardiovascular changes occur in pregnancy?

A

Raised:
Blood volume
Plasma volume
Cardiac output

Decreased:
Peripheral vascular resistance
BP (returns to normal by term)

Vasodilation- Causes flushing and hot sweats
Varicose veins

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41
Q

What respiratory changes occur in pregnancy?

A

Raised:
Tidal volume
RR

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42
Q

What renal changes occur in pregnancy?

A

Raised:
Blood flow
GFR
Sodium reabsorption
Water reabsorption
Protein excretion
Aldosterone- Increased salt/water reabsorption and retention

Physiological hydronephrosis

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43
Q

What changes occur in the blood in pregnancy?

A

Raised:
RBC production (higher iron, folate and B12 requirements)
Plasma volume increases more than RBC volume- Lower conc. RBCs
WBC
Clotting factor- Hypercoagulable- Increased risk VTE
ALP (placenta)
ESR and D-dimer
ALP- Due to secretion by placenta

Decreased:
Platelets
Albumin
Hb conc. and red cell conc.- Anaemia (due to high plasma volume)

Calcium requirements increase, but so does gut absorption of calcium- Stable

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44
Q

What changes can occur to the skin in pregnancy?

A

Linea nigra (increased melanocyte stimulating hormone)
Melasma
Striae gravidarum
Spider naevi
Palmar erythema
Pruritis- Can be normal or can indicate obstetric cholestasis
Postpartum hair loss- Normal, usually improves within 6mths

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45
Q

What changes occur in the female reproductive system during pregnancy?

A

Uterus- 100g increased to 1.1kg
Myometrium- Hypertrophy
Cervix- Increased discharge, ectropion
Vagina- Hypertrophy, increased discharge, candida, bacteria

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46
Q

What are the 3 stages of labour?

A

1st stage- Onset of labour (true contractions) until 10cm dilation
2nd stage- 10cm cervical dilation to delivery of baby
3rd stage- Delivery of baby to delivery of placenta

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47
Q

Outline the role of prostaglandins in pregnancy

A

Act like hormones
Stimulate contraction of uterine muscles
Ripen cervix before delivery

Pessaries containing prostaglandin E2 can be used to induce labour

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48
Q

What are Braxton-Hicks Contractions?

A

Occasional irregular contractions of uterus
Usually felt during second and third trimester
Can experience temporary and irregular tightening or mild cramping in abdomen
not true contractions- Don’t indicate onset of labour

Management- Stay hydrated and relax

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49
Q

Outline the 1st stage of labour

A

Onset of labour until cervix fully dilated (10cm)
Involves cervical dilation and effacement
Show- Mucus plug in cervix- Falls out

Latent phase
Active phase
Transition phase

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50
Q

What is the mucus plug?

A

The ‘show’
Prevents bacteria from entering uterus during pregnancy
Falls out during first stage of labour

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51
Q

What is the latent phase?

A

In first stage of labour
0-3cm dilation of cervix
Progresses at 0.5cm/h
Irregular contractions

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52
Q

What is the active phase?

A

3-7cm dilation of cervix
Progresses at 1cm/h
Regular contractions

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53
Q

What is the transition phase?

A

7-10cm dilation of cervix
Progresses at 1cm/h
Strong, regular contractions

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54
Q

Outline the 2nd stage of labour

A

10cm dilation to delivery of baby
- Power- Strength of uterine contractions
- Passenger- Size/attitude/lie/presentation
- Passage

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55
Q

What does attitude of the fetus mean?

A

Posture of fetus
Eg: How the back is rounded and how head and limbs are flexed

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56
Q

What does lie of the fetus mean?

A

Position of fetus in relation to mother’s body:
Longitudinal lie- Fetus straight up and down
Transverse lie- Fetus is straight side to side
Oblique lie- Fetus is at an angle

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57
Q

What does presentation of the fetus mean?

A

Part of fetus closest to cervix
Cephalic- head first
Shoulder- Shoulder first
Breech- Legs first- Complete (hips and knees flexed), Frank (hips flexed, knees extended, bottom first), Footling (foot hanging through cervix)

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58
Q

What are the cardinal movements of labour?

A

Engagement
Descent
Flexion
Internal rotation
Extension
Restitution and external rotation
Expulsion

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59
Q

Outline descent of the baby in labour

A

Position of baby’s head in relation to mother’s ischial spines during descent phase

-5 When baby is high up at pelvic inlet
0 Head is at ischial spines (head engaged)
+5 Fetal head has descended further out

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60
Q

Outline 3rd stage of labour

A

Completed birth of baby to delivery of placenta

Physiological management- Placenta delivered by maternal effort w/o meds or cord traction

Active management- Assisted delivery of placenta- Shortens 3rd stage and reduces risk of bleeding
Haemorrhage/>60min delay should prompt active management
Can be associated with nausea and vomiting

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61
Q

What is active management of third stage of labour?

A

Dose of IM oxytocin helps uterus contract and expel placenta
Careful traction applied to umbilical cord

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62
Q

What is amenorrhoea?

A

Lack of menstrual periods

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63
Q

What is primary amenorrhoea?

A

Patient never develops periods

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64
Q

List causes of primary amenorrhoea

A

Hypogonadotropic hypogonadism- Abnormal functioning of hypothalamus or pituitary gland
Hypergonadotropic hypogonadism- Abnormal functioning of gonads
Imperforate hymen or other structural pathology

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65
Q

What is secondary amenorrhoea?

A

Patient previously had periods that subsequently stopped

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66
Q

What are the causes of secondary amenorrhoea?

A

Pregnancy
Menopause
Physiological stress- Excessive exercise/low body weight/chronic disease/psychosocial factors
PCOS
Meds- Hormonal contraceptives
Premature ovarian insufficiency (menopause <40y)
Thyroid hormone abnormalities
Excessive prolactin (prolactinoma)
Cushing’s syndrome

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67
Q

What is anovulation?

A

Lack of ovulation

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68
Q

List the causes of irregular menstruation

A

Extremes of reproductive age (early periods or perimenopause)
PCOS
Physiological stress (excessive exercise/low body weight/chronic disease/psychosocial factors
Meds- Progesterone only contraception/antidepressants/antipsychotics
Hormonal imbalances- Thyroid abnormalities/Cushing’s syndrome/high prolactin

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69
Q

What are the causes of intermenstrual bleeding?

A

RED FLAG

Hormonal contraception
Cervical ectropion, polyps, cancer
STI
Endometrial polyps or cancer
Vaginal pathology- Including cancer
Pregnancy
Ovulation
Medications- SSRIs and anticoagulants

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70
Q

What is dysmenorrhoea?

A

Painful periods

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71
Q

What are the causes of dysmenorrhoea?

A

Primary dysmenorrhoea
Endometriosis or adenomyosis
Fibroids
PID
Copper coil
Cervical or ovarian cancer

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72
Q

What is menorrhagia?

A

Heavy menstrual bleeding

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73
Q

What are the causes of menorrhagia?

A

Dysfunctional uterine bleeding
Extremes of reproductive age
Fibroids
Endometriosis and adenomyosis
PID
Contraceptives- Copper coil
Anticoagulant meds
Bleeding disorders- VWD
Endocrine disorders- Diabetes and hypothyroidism
Connective tissue disorders
Endometrial hyperplasia or cancer
PCOS

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74
Q

What are the causes of postcoital bleeding?

A

RED FLAG

Cervical cancer, ectropion or infection
Trauma
Atrophic vaginitis
Polyps
Endometrial cancer
Vaginal cancer

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75
Q

What are the causes of pelvic pain?

A

UTI
Dysmenorrhoea
IBS
Ovarian cysts
Endometriosis
PID
Ectopic pregnancy
Appendicitis
Mittelschmerz
Pelvic adhesions
Ovarian torsion
IBD

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76
Q

What is Mittelschmerz?

A

Cyclical pain during ovulation

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77
Q

What are the causes of abnormal vaginal discharge?

A

Bacterial vaginosis
Candidiasis
Chlamydia
Gonorrhoea
Trichomonas vaginalis
Foreign body
Cervical ectropion
Polyps
Malignancy
Pregnancy
Ovulation (cyclical)
Hormonal contraception

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78
Q

What is pruritis vulvae?

A

Itching of vulva and vagina

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79
Q

What are the causes of pruritis vulvae?

A

Irritants (soaps, detergents, barrier contraception)
Atrophic vaginitis
Infection- Candidiasis/pubic lice
Eczema
Vulval malignancy
Pregnancy-related
Urinary or fecal incontinence
Stress

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80
Q

What are the definitions of primary amenorrhoea?

A

Not starting menstruation:
By 13y if no other signs of pubertal development
By 15y if other signs of puberty

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81
Q

What is hypogonadism?

A

Lack of sex hormones/oestrogen/testosterone
Hypogonadotropic hypogonadism- LH and FSH deficiency
Hypergonadotropic hypogonadism- Lack of response to LH and FSH by gonads

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82
Q

What is hypogonadotropic hypogonadism?

A

Deficiency of LH and FSH leading to deficiency of sex hormones
Result of abnormal functioning of hypothalamus or pituitary gland

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83
Q

What are LH and FSH?

A

Gonadotrophins produced by anterior pituitary gland in response to gonadotropin releasing hormone (GnRH)

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84
Q

What can cause hypogonadotropic hypogonadism?

A

Hypopituitarism
Damage to hypothalamus or pituitary
Sig. chronic conditions- CF or IBD
Excessive dieting or exercise
Constitutional delay in growth and development
Endocrine disorders- GH deficiency, hypothyroidism, Cushing’s, hyperprolactinaemia
Kallman syndrome

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85
Q

What is Hypergonadotropic hypogonadism?

A

Gonads fail to respond to LH and FSH
Anterior produces high levels of LH and FSH and low sex hormones

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86
Q

What can cause hypergonadotropic hypogonadism?

A

Previous damage to gonads (torsion, cancer, infections (mumps))
Congenital absence of ovaries
Turner’s syndrome

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87
Q

What is Kallman syndrome?

A

Genetic condition
Causes hypogonadotrophic hypogonadism
Failure to start puberty
Associated with anosmia (absent sense of smell)

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88
Q

What is congenital adrenal hyperplasia?

A

Congenital deficiency of 21-hydroxylase enzyme
Underproduction of cortisol and aldosterone and overproduction of androgens from birth
Autosomal recessive

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89
Q

How does congenital adrenal hyperplasia present?

A

Severe- Neonate unwell shortly after birth- Electrolyte disturbances and hypoglycaemia

Females:
Tall for age
Facial hair
Absent periods (primary amenorrhoea)
Deep voice
Early puberty

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90
Q

What is androgen insensitivity syndrome?

A

Tissues unable to respond to androgen hormones (testosterone)
Typical male sexual characteristics don’t develop
Results in female phenotype- Other than internal pelvic organs
Normal external genitalia and breast tissue
Internally- Testes, absent uterus/upper vagina/fallopian tubes/ovaries

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91
Q

List structural pathology causes of primary amenorrhoea

A

Imperforate hymen
Transverse vaginal septae
Vaginal agenesis
Absent uterus
Female genital mutilation

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92
Q

Outline investigations of primary amenorrhoea

A

Anaemia- FBC, ferritin
CKD- U&Es
Coeliac disease- Anti-TTG, anti-EMA antibodies

Hormonal bloods:
FSH and LH
TFTs
GH deficiency screening- ILGF-1
Hyperprolactinaemia- Prolactin raised
Raised testosterone- PCOS, androgen insensitivity syndrome, congenital adrenal hyperplasia

Genetic testing with microarray- Turner’s syndrome

Imaging:
Xray wrist- Constitutional delay
Pelvic US- Ovaries and pelvic organs
MRI brain- Assess olfactory bulbs in possible Kallman syndrome

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93
Q

How is hypogonadotrophic hypogonadism managed?

A

Pulsatile GnRH to induce ovulation and menstruation
Or can replace sex hormones- COCP

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94
Q

What is the definition of secondary amenorrhoea?

A

No menstruation >3mths after regular periods
Investigate after 3-6mths

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95
Q

What are the causes of secondary amenorrhoea?

A

Pregnancy
Menopause and premature ovarian failure
Hormonal contraception (IUS or POP)
PCOS
Asherman’s syndrome
Thyroid pathology
Hyperprolactinaemia
Pituitary tumours- Prolactin-secreting prolactinoma
Pituitary failure- Trauma/radiotherapy/surgery/Sheehan syndrome
Excessive exercise/low body weight/ED/chronic disease/psychological stress

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96
Q

What is hyperprolactinaemia?

A

High prolactin levels act on hypothalamus to prevent release of GnRH
No GnRH= No LH and FSH- Hypogonadotrophic hypogonadism

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97
Q

What is galactorrhoea associated with?

A

Is breast milk production and secretion
Hyperprolactinaemia
High prolactin level

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98
Q

What is the most common cause of hyperprolactinaemia?

A

Pituitary adenoma secreting prolactin

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99
Q

How is hyperprolactinaemia managed?

A

Often no treatment
Dopamine agonists- Bromocriptine or cabergoline- Can reduce prolactin production

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100
Q

What can bromocriptine and cabergoline be used to treat?

A

(Dopamine agonists)

Hyperprolactinaemia
Parkinson’s disease
Acromegaly

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101
Q

Outline investigations of secondary amenorrhoea

A

Hormonal blood tests
US pelvis to diagnose PCOS

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102
Q

Which hormone tests are done in secondary amenorrhoea?

A

bHCG- Pregnancy

LH and FSH:
High FSH- Primary ovarian failure
High LH, or LH:FSH ratio- PCOS

Prolactin- Hyperprolactinaemia
Follow with MRI- Pituitary tumour

TSH
Follow with T3 and T4 if abnormal
High TSH, low T3 and T4- Hypothyroidism
Low TSH, high T3 and T4- Hyperthyroidism

Raised testosterone- PCOS, androgen insensitivity syndrome or congenital adrenal hyperplasia

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103
Q

Why does PCOS require a withdrawal bleed every 3-4mths when managing and why?

A

Reduce risk endometrial hyperplasia/cancer
Medroxyprogesterone for 14d, or regular use of COCP- Stimulate withdrawal bleed

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104
Q

Outline association between secondary amenorrhoea and osteoporosis

A

Amenorrhoea associated with low oestrogen- Increased risk osteoporosis
Treat if amenorrhoea >12mths

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105
Q

How is risk of osteoporosis managed in secondary amenorrhoea?

A

Vit D and calcium
HRT or COCP

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106
Q

What is premenstrual syndrome?

A

Psychological/emotional/physical symptoms during luteal phase of menstrual cycle
Resolve once menstruation begins
Not present before menarche/during pregnancy/after menopause

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107
Q

Outline presentation of PMS

A

Low mood
Anxiety
Mood swings
Irritability
Bloating
Fatigue
Headaches
Breast pain
Reduced confidence
Cognitive impairment
Clumsiness
Reduced libido

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108
Q

When can PMS continue in absence of periods?

A

Hysterectomy
Endometrial ablation
Mirena

Ovaries continue to function and hormonal cycle continues

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109
Q

What is progesterone-induced premenstrual disorder?

A

Symptoms of PMS occurring in response to taking meds containing progesterone
COCP or cyclical-HRT

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110
Q

How is PMS diagnosed?

A

Symptoms diary spanning 2 menstrual cycles
Definitive- Administer GnRH analogues and temporarily induce menopause to see if symptoms resolve

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111
Q

Outline management of PMS

A

Lifestyle- Diet/exercise/alcohol/smoking/stress/sleep
COCP- Drospirenone
SSRI antidepressants
CBT
Continuous transdermal oestrogen (patch)- Requires progesterone endometrial protection alongside (norethisterone/mirena coil) to trigger withdrawal bleed
GnRH analogues- Induce menopausal state
Hysterectomy and bilateral oopherectomy- HRT will be required
Danazole and tamoxifen- Cyclical breast pain
Spironolactone- Breast swelling, water retention, bloating

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112
Q

What are the potential SEs of GnRH analogues?

A

Osteoporosis
Add HRT to mitigate effects

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113
Q

What investigations should be done in menorrhagia?

A

Pelvic exam with speculum and bimanual
FBC- Iron deficiency anaemia
Outpatient hysteroscopy- If suspected submucosal fibroids/suspected endometrial pathology/persistent intermenstrual bleeding
Pelvic and transvaginal US- If possible large fibroid/adenomyosis/exam difficult to interpret (obesity)/hysteroscopy declined

Swabs- If evidence infection
Coagulation screen- FH clotting disorders
Ferritin- Clinically anaemic
TFTs- Features of hypothyroidism

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114
Q

Outline management of menorrhagia

A

No contraception:
TXA (if no pain)
Mefenamic acid (if associated pain)

Contraception:
1. Mirena coil
2. COCP
3. Cyclical oral progestogens- Norethisterone

Refer to secondary care

Surgical:
Endometrial ablation
Hysterectomy

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115
Q

What are fibroids?

A

Benign tumours of smooth muscle of uterus
Oestrogen sensitive- Grow in response to oestrogen

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116
Q

List the types of fibroids in the uterus

A

Intramural- Within myometrium- Can change shape and distort uterus
Subserosal- Just below outer layer of uterus- Grow out, can be very large filling abdomen
Submucosal- Just below endometrium
Pedunculated- Stalk

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117
Q

Outline symptoms of Fibroids

A

Often asymptomatic
Heavy menstrual bleeding most common
Prolonged menstruation (>7d)
Abdominal pain- Worse during menstruation
Bloating/feeling full in abdo
Urinary/bowel symptoms due to pelvic pressure/fullness
Deep dyspareunia
Reduced fertility

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118
Q

Outline investigations of PCOS

A

Hysteroscopy- Initial investigation
Pelvic US
MRI scanning

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119
Q

Outline management of fibroids <3cm

A

1st line- Mirena coil
NSAIDs and TXA
COCP
Cyclical oral progestogens

Surgical:
Endometrial ablation
Resection of submucosal fibroids during hysteroscopy
Hysterectomy

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120
Q

Outline management of fibroids >3cm

A

NSAIDs and TXA
Mirena coil
COCP
Cyclical oral progestogens

Surgical:
Uterine artery embolisation
Myomectomy
Hysterectomy

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121
Q

What can be used to reduce size of fibroids before surgery?

A

GnRH agonists- Goserelin or leuprorelin

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122
Q

What are the complications of fibroids?

A

Heavy menstrual bleeding- Iron deficiency anaemia
Reduced fertility
Pregnancy complications- Miscarriages, premature labour, obstructive delivery
Constipation
Urinary outflow tract obstruction and UTI
Red degeneration of fibroid
Torsion of fibroid (pedunculated)
Malignant change to leiomyosarcoma (rare)

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123
Q

What is red degeneration of fibroid?

A

Ischaemia, infarction and necrosis of fibroid due to disrupted blood supply
More likely to occur in large fibroids during 2nd/3rd trimester pregnancy

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124
Q

How does red degeneration of fibroid present?

A

Severe abdo pain
Low grade fever
Tachycardia
Vomiting

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125
Q

How is red degeneration of fibroid managed?

A

Supportive
Rest
Fluids
Analgesia

126
Q

What is endometriosis?

A

Ectopic endometrial tissue outside uterus

127
Q

What is adenomyosis?

A

Endometrial tissue within myometrium of uterus
More common in later reproductive years and in multiparous women

128
Q

What is the main symptom of endometriosis?

A

Pelvic pain
Endometrial cells outside uterus also shed lining and bleed
Deposits in bladder/bowel- Blood in urine/stools
Localised bleeding and inflammation lead to adhesions- Fixes structures together

129
Q

What are the key symptoms of adhesions in endometriosis?

A

Chronic, non-cyclical pain
May be sharp/stabbing/pulling and associated with nausea

130
Q

Outline presentation of endometriosis

A

Cyclical abdo/pelvic pain
Deep dyspareunia
Dysmenorrhoea
Infertility
Cyclical haematuria/blood in stools
Urinary/bowel symptoms

131
Q

Outline potential signs on examination in endometriosis

A

Endometrial tissue visible in vagina on speculum (posterior fornix)
Fixed cervix on bimanual
Tenderness in vagina/cervix/adnexa

132
Q

Outline diagnosis of endometriosis

A

Pelvic US
Laparoscopic surgery- Gold standard

133
Q

Outline staging of endometriosis

A

Stage 1: Small superficial lesions
Stage 2: Mild, deeper lesions
Stage 3: Deeper lesions, lesions on ovaries and mild adhesions
Stage 4: Deep and large lesions affecting ovaries with extensive adhesions

134
Q

Outline management of endometriosis

A

Analgesia as required
COCP- Can be used back to back
POP
Depo injection
Nexplanon implant
Mirena coil
GnRH agonists

Surgical:
Laparoscopic surgery- Excise or ablate
Hysterectomy

135
Q

Which management of endometriosis may improve fertility?

A

Laparoscopic treatment

136
Q

Outline presentation of adenomyosis

A

Dysmenorrhoea
Menorrhagia
Dyspareunia

Infertility
Enlarged tender uterus- Softer than in fibroids

137
Q

Outline diagnosis of adenomyosis

A

Transvaginal US
MRI and transabdominal US
Gold standard- Histological exam of uterus after hysterectomy

138
Q

Outline management of adenomyosis

A

No contraception:
TXA (antifibrinolytic)- If no associated pain
Mefenamic acid- Pain

Contraception:
1. Mirena coil
2. COCP
3. Cyclical oral progestogens

Others:
GnRH analogue
Endometrial ablation
Uterine artery embolisation
Hysterectomy

139
Q

Outline the link between pregnancy and adenomyosis

A

Infertility
Miscarriage
Preterm birth
SGA
Preterm PROM
Malpresentation
Need for CS
PPH

140
Q

What is menopause?

A

Permanent end to menstruation
No periods for 12mths

141
Q

When is someone described as postmenopausal?

A

12mths after final menstrual period onwards

142
Q

When is someone described as perimenopausal?

A

Time leading up to last period and the 12mths after
May experience vasomotor symptoms and irregular periods
Typically >45y

143
Q

What happens to levels of sex hormones during meopause?

A

Oestrogen and progesterone- Low
LH and FSH- High (due to absence negative feedback from oestrogen)

144
Q

Outline physiology of menopause

A

Decline in development of ovarian follicles- Reduced production oestrogen
Low oestrogen- High LH and FSH, endometrium doesn’t develop (amenorrhoea)
Ovulation doesn’t occur- Irregular menstruation

145
Q

What causes perimenopausal symptoms?

A

Low oestrogen

146
Q

List some perimenopausal symptoms

A

Hot flushes
Emotional lability/low mood
Premenstrual syndrome
Irregular periods
Joint pains
Heavier/lighter periods
Vaginal dryness and atrophy
Reduced libido

147
Q

What does low oestrogen increase risk of?

A

CVD and stroke
Osteoporosis
Pelvic organ prolapse
Urinary incontinence

148
Q

Outline diagnosis of menopause

A

> 45y with typical symptoms

FSH blood test:
Women <40y with suspected premature menopause
Women 40-45y menopausal symptoms/change in menstrual cycle

149
Q

Outline contraception around menopause

A

Need contraception for:
2y after last period <50y
1y after last period >50y

150
Q

Which contraceptive methods are recommended for women approaching menopause?

A

UKMEC1:
Barrier
Mirena/copper coil
POP
Progesterone implant
Progesterone depot injection (<45y)
Sterilisation

COCP- UKMEC2- Use COCP containing norethisterone or levonorgestrel >40y (lower risk VTE)

151
Q

What are the SEs of depo-provera injection?

A

Weight gain
Reduced bone mineral density (osteoporosis)

152
Q

How are perimenopausal symptoms managed?

A

Vasomotor symptoms likely to resolve after 2-5y
No treatment
HRT
Tibolone- Synthetic steroid hormone- Continuous combined HRT- Only after 12mths amenorrhoea
Clonidine
SSRI- Fluoxetine or citalopram
Testosterone- Treat reduced libido
Vaginal oestrogen cream/tablet- Helps vaginal dryness and atrophy
Vaginal moisturisers

153
Q

What is premature ovarian insufficiency?

A

Menopause <40y

154
Q

How is premature ovarian insufficiency characterised?

A

Hypergonadotropic hypogonadism

Raised LH and FSH
Low oestradiol

155
Q

What are the causes of premature ovarian syndrome?

A

Idiopathic
Iatrogenic- Chemo/radiotherapy/surgery
AI- Coeliac disease, adrenal insufficiency, T1D, thyroid disease
Genetic- FH, Turners
Infections- Mumps, TB, CMV

156
Q

Outline presentation of premature ovarian syndrome

A

Irregular/lack of periods <40y
Symptoms of low oestrogen- Hot flushes, night sweats, vaginal dryness

157
Q

How is premature ovarian syndrome diagnosed?

A

<40y
Typical menopausal symptoms
Elevated FSH (raised on 2 tests 4wks apart)

158
Q

Outline management of premature ovarian syndrome

A

HRT until age of menopause:
Traditional HRT- Lowers BP
COCP

159
Q

What are the risks associated with premature ovarian syndrome?

A

CVD
Osteoporosis
Cognitive and psychological risks

160
Q

What is the risk of taking HRT >50y?

A

Breast cancer

161
Q

What is the risk of taking HRT <50y?

A

VTE
Reduce risk with transdermal patch

162
Q

Outline HRT

A

Used in perimenopausal/postmenopausal symptoms associated with low oestrogen
Progesterone needs to be given to women with a uterus- Prevents endometrial hyperplasia/cancer

163
Q

Which women need continuous combined HRT?

A

Postmenopausal with uterus and >12mths no periods- Requires progesterone protection

164
Q

Which women can take oestrogen-only HRT?

A

Without uterus

165
Q

Which women should take cyclical HRT?

A

Still having periods

Should also have cyclical progesterone and regular breakthrough bleeds

166
Q

Outline non-hormonal treatments for menopausal symptoms

A

Improve diet, exercise, weight loss, smoking cessation, reduce alcohol, reduce caffeine, reduce stress
CBT
Clonidine
SSRI- Fluoxetine
SNRI- Venlafaxine
Gabapentin

167
Q

How does clonidine work?

A

Agonist of alpha-2 adrenergic receptors and imidazoline receptors in brain
Lowers BP and HR
Reduces vasomotor symptoms and hot flushes

168
Q

What are the SEs of clonidine?

A

Dry mouth
Headaches
Dizziness
Fatigue

Sudden withdrawal- Raises BP, agitation

169
Q

List alternative remedies for menopausal symptoms

A

Black cohosh
Dong quai
Red clover
Evening primrose oil
Ginseng

170
Q

What are the SEs of black cohosh?

A

Liver damage

171
Q

What are the SEs of Dong quai?

A

Cause bleeding disorders

172
Q

What are the SEs of Red Clover?

A

Oestrogenic effects- Concerning in oestrogen sensitive cancers

173
Q

What are the SEs of Evening Primrose Oil?

A

Significant drug interactions
Linked with clotting disorders and seizures

174
Q

What are the SEs of Ginseng?

A

Mood and sleep benefits

175
Q

What are the indications for HRT?

A

Replacing hormones in premature ovarian insufficiency
Reduce vasomotor symptoms
Improve low mood/decreased libido/poor sleep/joint pain
Reduce risk osteoporosis <60y

176
Q

What are the benefits of HRT in <60y?

A

Improved vasomotor and symptoms of menopause
Improved QoL
Reduce risk osteoporosis and fractures

177
Q

What are the risks of taking HRT?

A

Older women with increased duration:
Breast cancer
Endometrial cancer
VTE
Stroke and coronary artery disease

No increased risk <50y
No risk endometrial cancer if no uterus
No increased risk CAD in oestrogen-only HRT

Can have unscheduled bleeding in first 3-6mths- Investigate after this (endometrial cancer)

178
Q

What are the CIs to HRT?

A

Undiagnosed abnormal bleeding
Endometrial hyperplasia/cancer
Breast cancer
Uncontrolled HTN
VTE
Liver disease
Active angina/MI
Pregnancy

179
Q

What are the options for delivering progesterone with HRT?

A

Oral tablets
Transdermal patches
IUS (Mirena)

180
Q

What is Tibolone?

A

Helps patients with reduced libido
Used as form of continuous combined HRT- Must be postmenopausal
Synthetic steroid that stimulates oestrogen and progesterone receptors

181
Q

What is the role of testosterone transdermal patches in menopause?

A

Improves energy levels and sex drive

182
Q

What should patients taking oestrogen-containing contraceptives or HRT do before major surgery?

A

Stop 4wks before

183
Q

What are the oestrogenic SEs of HRT?

A

Nausea and bloating
Breast swelling
Breast tenderness
Headaches
Leg cramps

184
Q

What are the progestogenic SEs HRT?

A

Mood swings
Bloating
Fluid retention
Weight gain
Acne and greasy skin

185
Q

How should HRT be stopped?

A

No specific regime
Can reduce slowly if prefer to reduce risk of symptoms suddenly recurring

186
Q

Outline Rotterdam criteria

A

Diagnosing PCOS

Oligoovulation/anovulation- Irregular/absent periods
Hyperandrogenism- Hirsutism and acne
Polycystic ovaries on US (or ovarian volume >10cm3)

187
Q

Outline presentation of PCOS

A

Oligomenorrhoea or amenorrhoea
Infertility
Obesity
Hirsutism
Acne
Hair loss in male pattern

188
Q

Outline additional features of PCOS

A

Insulin resistance and diabetes
Acanthosis nigricans
CVD
Hypercholesterolaemia
Endometrial hyperplasia and cancer
OSA
Depression and anxiety
Sexual problems

189
Q

What is acanthosis nigricans?

A

Thickened, rough skin
In axilla and on elbows
Velvety texture
Occurs with insulin resistance

190
Q

List causes of Hirsuitism

A

Meds- Phenytoin, ciclosporin, corticosteroids, testosterone, anabolic steroids
Ovarian/adrenal tumours that secrete androgens
Cushing’s syndrome
PCOS
Congenital adrenal hyperplasia

191
Q

Outline insulin resistance and PCOS

A

Resistance to insulin- Produce more insulin
Insulin promotes release of androgens from ovaries and adrenal glands
Insulin supresses sex hormone-binding globulin (SHBG) produced by liver- Normally suppresses androgens function- Low SHBG promotes hyperandrogenism
High insulin- Halts follicle development in ovaries- Anovulation and multiple partially developed follicles on scan

192
Q

Outline investigations of PCOS

A

Bloods:
Testosterone- Raised
Sex hormone-binding globulin (SHBG)- Low
LH- High
FSH
LH:FSH- High LH compared to FSH
Raised insulin
Mildly elevated prolactin
TSH
Normal/raised oestrogen

Pelvic US- Transvaginal- String of pearls

OGTT

193
Q

What is the characteristic description of PCOS on TV US?

A

String of pearls around periphery of ovary

194
Q

Outline how to interpret OGTT

A

Impaired fasting glucose: Fasting glucose 6.1-6.9 mmol/l (before glucose drink)
Impaired glucose tolerance: Plasma glucose at 2h 7.8-11.1mmol/l
Diabetes: Plasma glucose at 2h >11.1mmol/l

195
Q

Outline general management of PCOS

A

Weight loss
Low glycaemic index, calorie-controlled diet
Exercise
Smoking cessation
Antihypertensive meds if required
Statins if indicated (QRISK >10%)

196
Q

Outline orlistat

A

Can help weight loss in women BMI >30
Lipase inhibitor that stops absorption of fat in intestines

197
Q

How is the risk of endometrial cancer managed in PCOS?

A

Less frequent menstruation- Don’t produce enough progesterone- Endometrial lining proliferates

If extended gap between periods (>3mths) or abnormal bleeding- Pelvic US and assess endometrial thickness- Use cyclical progestogens prior to scan
Endometrial thickness >10mm- Biopsy

198
Q

What are the risk factors for endometrial cancer in PCOS?

A

Obesity
Diabetes
Insulin resistance
Amenorrhoea

199
Q

What are the options for reducing risk of endometrial cancer in PCOS?

A

Mirena coil- Continuous endometrial protection
Induce withdrawal bleed at least every 3-4mths:
Cyclical progestogens
COCP

200
Q

How is infertility managed in PCOS?

A

Weight loss
Clomifene
Laparoscopic ovarian drilling
IVF
Metformin and letrozole
Ovarian drilling- Laparoscopic surgery

If become pregnant- Screen for gestational diabetes (OGTT)

201
Q

How is hirsutism managed in PCOS?

A

Weight loss
Co-cyprindiol (Dianette)- For acne also- 3x increased risk VTE
Topical eflornithine (facial)- Takes 6wks to improve- Once stopped hirsutism recurs
Electrolysis
Laser hair removal
Spironolactone
Finasteride
Flutamide
Cyproterone acetate

202
Q

How is acne managed in PCOS?

A

COCP- 1st line
Topical adapalene
Topical ABs (clindamycin and benzoyl peroxide)
Topical azelaic acid
Oral tetracyclines (eg: Lymecycline)

203
Q

Outline ovarian cysts

A

Fluid filled sac
Functional ovarian cyst- Related to fluctuating hormones in menstrual cycle- Common premenopausal

Postmenopausal cysts- More concerning for malignancy

204
Q

Outline presentation of ovarian cysts

A

Mostly asymptomatic
Pelvic pain
Bloating
Fullness in abdomen
Palpable pelvic mass

Acute pelvic pain- Torsion, haemorrhage or rupture

205
Q

What are the types of functional ovarian cysts?

A

Follicular- On developing follicle- If don’t rupture and release egg, can persist- Harmless and disappear after a few menstrual cycles
Corpus luteum- Occur when corpus luteum fails to breakdown- Often seen in early pregnancy

206
Q

What are serous cystadenomas?

A

Ovarian cyst
Benign tumour of epithelial cells

207
Q

What are mucinous cystadenomas?

A

Ovarian cyst
Benign tumour of epithelial cells
Can become huge- Take up lots of space in pelvis and abdomen

208
Q

What are endometriomas?

A

‘Chocolate cyst’
Sign of endometriosis

209
Q

What are dermoid cysts/Germ cell tumours?

A

Benign ovarian tumour
Teratomas
Contain various tissue types- Skin/teeth/hair
Particularly associated with ovarian torsion

210
Q

What are sex cord-stromal tumours?

A

Rare ovarian cyst
Can be malignant or benign
Arise from stroma or sex cords

211
Q

What are the symptoms associated with ovarian cysts that may suggest malignancy?

A

Abdominal bloating
Reduced appetite
Early satiety
Weight loss
Urinary symptoms
Pain
Ascites
Lymphadenopathy

212
Q

List the risk factors of ovarian cancer

A

Reduced number of ovulations:
Later onset of periods
Early menopause
Any pregnancy
COCP

213
Q

What are the causes of raised CA125?

A

Ovarian cancer
Endometriosis
Fibroids
Adenomyosis
Pelvic infection
Liver disease
Pregnancy

214
Q

Outline blood tests to be done to investigate ovarian cysts

A

Premenopausal with simple ovarian cysts <5cm on US don’t require further investigations

CA125- Tumour marker for ovarian cancer

Women <45y complex ovarian mass (tumour markers for possible germ cell tumour):
Lactate dehydrogenase
Alpha-fetoprotein
HCG

215
Q

What is the Risk of Malignancy Index (RMI)?

A

Estimates risk of ovarian mass being malignant

Menopausal status
US findings
CA125 level

216
Q

What is Meig’s syndrome?

A

Triad:
Ovarian fibroma
Pleural effusion
Ascites

Older women
Remove tumour- Complete resolution of effusion and ascites

217
Q

What are the complications of ovarian cysts?

A

Torsion
Haemorrhage
Rupture

218
Q

Outline management of ovarian cysts

A

Possible ovarian cancer- 2wk wait
Dermoid cyst- Refer and consider surgery
Persistent/enlarging- Surgical intervention

Simple in premenopause:
<5cm discharge
5-7cm- Refer and yrly US monitoring
>7cm- Consider MRI/surgery

219
Q

What is ovarian torsion?

A

Ovary twists in relation to surrounding connective tissue, fallopian tube and blood supply (adnexa)
Usually due to ovarian mass >5cm (cyst/tumour)
More likely to occur with benign tumours and in pregnancy

220
Q

What is the risk of ovarian torsion?

A

Ischaemia and necrosis if persists
Function of ovary lost- EMERGENCY

221
Q

Outline presentation of ovarian torsion

A

Sudden onset severe unilateral pelvic pain
Constant, gets progressively worse
Nausea and vomiting
Can potentially twist and untwist- Fluctuating symptoms
Localised tenderness on examination and possibly palpable mass

222
Q

Outline diagnosis of ovarian torsion

A

Pelvic US- Whirlpool sign, free fluid in pelvis and oedema of ovary
Definitive- Laparoscopic surgery

223
Q

Outline management of ovarian torsion

A

Emergency admission
Laparoscopic surgery- To untwist or remove ovary

224
Q

What are the complications of ovarian torsion?

A

Ovary becomes necrotic and not removed- Infection- Abscess- Sepsis
At rupture- Peritonitis and adhesions

225
Q

What is Asherman’s syndrome?

A

Adhesions within uterus following damage to uterus

226
Q

What are the risk factors for Asherman’s syndrome?

A

Pregnancy-related dilatation and curretage
Treatment of retained products of conception
Uterine surgery
Pelvic infection
Endometrial curretage

227
Q

Outline presentation of Asherman’s syndrome

A

Presents following exposure to RFs
Secondary Amenorrhoea
Sig. lighter periods
Dysmenorrhoea
Infertility

228
Q

Outline diagnosis of Asherman’s syndrome

A

Hysteroscopy- Gold standard
Hysterosalpingography
Sonohysterography
MRI

229
Q

Outline management of Asherman’s syndrome

A

Dissection of adhesions during hysteroscopy
Reoccurrence common

230
Q

What is cervical ectropion?

A

Columnar epithelium of endocervix extends into stratified squamous epithelium of ectocervix
Lining of endocervix becomes becomes visible on examination
Cells of endocervix more fragile and prone to trauma (postcoital bleeding)

231
Q

What are the risk factors for developing cervical ectropion?

A

Associated with higher oestrogen levels:
Younger women
COCP
Pregnancy

232
Q

What is the transformation zone in cervical ectropion?

A

Border between columnar epithelium of endocervix and stratified squamous epithelium of ectocervix

233
Q

Outline presentation of cervical ectropion

A

Often asymptomatic
Increased vaginal discharge
Vaginal bleeding
Dyspareunia
Postcoital bleeding
Exam- Well demarcated border between redder velvety columnar epithelium extending from os, and pale pink squamous epithelium of ectocervix

234
Q

What is the association between cervical ectropion and cervical cancer?

A

No association
Always ask about smears

235
Q

Outline management of cervical ectropion

A

Asymptomatic- No treatment, resolves as get older/stop pill/not pregnant
Not a CI to COCP

Problematic bleeding- Cauterise with silver nitrate or cold coagulation during colposcopy

236
Q

What are Nabothian cysts?

A

Fluid filled cysts on surface of cervix
Up to 1cm size

237
Q

What is the association between Nabothian cysts and cervical cancer?

A

No association

238
Q

What are the risk factors for developing Nabothian cysts?

A

Childbirth
Minor trauma to cervix
Cervicitis

239
Q

Outline presentation of Nabothian cysts

A

Often found incidentally on speculum exam
Don’t typically cause symptoms
If very large, may cause feeling of fullness in pelvis
Have whitish/yellow appearance

240
Q

Outline management of Nabothian cysts

A

Diagnosis clear- Reassure, no treatment, often resolve
Uncertain- Refer for colposcopy, may excise or biopsy

241
Q

What is a uterine prolapse?

A

Uterus descends in to vagina

242
Q

What is a vault prolapse?

A

Occurs if had hysterectomy
Top of vagina descends into vagina

243
Q

What is a rectocele?

A

Defect in posterior vaginal wall
Rectum prolapses forward into vagina
Associated with constipation

244
Q

What are the symptoms of faecal loading in a rectocele?

A

Significant constipation
Urinary retention (compression on urethra)
Palpable lump in vagina
Women may use fingers to press lump back in to open bowels

245
Q

What is a cystocele?

A

Defect in anterior vaginal wall
Bladder prolapses back into vagina

246
Q

What are the risk factors for prolapse?

A

Multiple vaginal deliveries
Instrumental/prolonged/traumatic delivery
Advanced age and postmenopause status
Obesity
Chronic respiratory disease causing coughing
Chronic constipation causing straining

247
Q

Outline presentation of prolapse

A

Feeling of something coming down in vagina
Dragging/heavy sensation in pelvis
Urine- Urinary incontinence, urgency, frequency, weak stream, retention
Bowel- Constipation, incontinence and urgency
Sexual dysfunction- Pain, altered sensation, reduced enjoyment

248
Q

Outline examination of prolapse

A

Empty bladder and bowel before examination
Sim’s speculum
Ask to cough or bear down

249
Q

Outline grades of uterine prolapse

A

Grade 0: Normal
Grade 1: Lowest part >1cm above introitus
Grade 2: Lowest part within 1cm of introitus
Grade 3: Lowest part >1cm below introitus but not fully descended
Grade 4: Full descent with eversion of vagina

Uterus descending beyond introitus- Uterine procidentia

250
Q

Outline conservative management of uterine prolapse

A

Pelvic floor exercises
Weight loss
Associated stress incontinence- Reduce caffeine intake and incontinence pads
Vaginal oestrogen cream

251
Q

Outline use of vaginal pessaries in managing uterine prolapse

A

Insert into vagina and change every 4mths

Ring
Shelf and Gellhorn- Flat disc with stem
Cube
Donut
Hodge- Rectangular

252
Q

Outline surgical options for uterine prolapse

A
253
Q

What are the possible complications of uterine prolapse surgery?

A

Pain, bleeding, infection, DVT, risk of anaesthetic
Damage to bladder/bowel
Recurrence of prolapse
Altered experience of sex

254
Q

What are the potential complications of mesh repairs in uterine prolapse?

A

No longer used

Chronic pain
Altered sensation
Dyspareunia
Abnormal bleeding
Urinary/bowel problems

255
Q

Outline urge incontinence

A

Overactivity of detrusor muscle of bladder
Feel sudden urge to pass urine

256
Q

Outline stress incontinence

A

Weakness of pelvic floor
Urine leaks when increased pressure- Coughing/laughing/surprised

257
Q

Outline mixed incontinence

A

Combination of urge and stress incontinence

258
Q

Outline overflow incontinence

A

Chronic urinary retention due to obstruction to outflow of urine

259
Q

What are the causes of overflow incontinence?

A

Anticholinergic meds
Fibroids
Pelvic tumours
Neuro- MS, diabetic neuropathy, spinal cord injury

More common in men (rare in women)

260
Q

How is overflow incontinence diagnosed?

A

Urodynamic testing

261
Q

What are the risk factors for urinary incontinence?

A

Increased age
Postmenopausal status
High BMI
Previous pregnancies and vaginal deliveries
Pelvic organ prolapse
Pelvic floor surgery
MS
Cognitive impairment and dementia

262
Q

How is strength of pelvic muscle contractions assessed?

A

Bimanual exam

0: No contraction
1: Faint contraction
2: Weak contraction
3: Moderate contraction with some resistance
4: Good contraction with resistance
5: Strong contraction, firm squeeze and drawing inwards

263
Q

Outline investigations of urinary incontinence

A

Bladder diary over at least 3d
Urine dipstick testing
Post-voidal residual bladder volume
Urodynamic testing- Investigate urge incontinence not responding to 1st line meds/difficulty urinating/urinary retention/previous surgery/unclear diagnosis

264
Q

Outline urodynamic tests

A

Stop taking anticholinergic meds 5d before test
Thin catheter in bladder and rectum- Measure pressures in bladder and rectum

Cystometry- Measures detrusor muscle contraction and pressure
Uroflowmetry- Measures flow rate
Leak point pressure- Point at which urine leaks
Post-void residual bladder volume- Incomplete emptying
Video urodynamic testing- Fill bladder with contrast and take xray

265
Q

Outline management of stress incontinence

A

Avoid caffeine/diuretics/overfilling bladder
Avoid excessive/restricted fluid intake
Weight loss
Supervised pelvic floor exercises- 3mths
Surgery
Duloxetine- SNRI (2nd line if surgery less preferred)

266
Q

Outline surgical options for managing stress incontinence

A

Tension-free vaginal tape
Autologous sling procedures
Colposuspension
Intramural urethral bulking

267
Q

Outline management of urge incontinence

A

Bladder retraining- 6wks
Anticholinergic meds- Oxybutynin/tolterodine/solifenacin
Mirabegron
Botulinum toxin type A- Inject in bladder wall
Percutaneous sacral nerve stimulation
Augmentation cystoplasty
Urinary diversion

268
Q

What are the anticholinergic SEs?

A

Dry mouth
Dry eyes
Urinary retention
Constipation
Postural hypotension
Cognitive decline, memory problems, worsening of dementia

269
Q

What are the CIs of mirabegron?

A

Uncontrolled HTN
Monitor BP regularly
Can lead to hypertensive crisis and increased risk TIA and stroke

270
Q

What is atrophic vaginitis?

A

Dryness and atrophy of vaginal mucosa
Related to lack of oestrogen
Occurs in menopause
Epithelial lining usually thickens/elastic/produces secretions in response to oestrogen
Tissue more prone to inflammation
Changes in vaginal pH and microbial flora- Infections
Low oestrogen can also lead to prolapse and stress incontinence (affects health of CT)

271
Q

Outline presentation of atrophic vaginitis

A

Postmenopausal
Itching
Dryness
Dyspareunia
Bleeding due to localised inflammation
Recurrent UTIs
Stress incontinence
Prolapse

272
Q

Outline findings on examination of atrophic vaginitis

A

Pale mucosa
Thin skin
Reduced skin folds
Erythema and inflammation
Dryness
Sparse pubic hair

273
Q

Outline management of atrophic vaginitis

A

Vaginal lubricants
Estriol cream/pessaries
Estradiol tablets/ring

274
Q

What are the CIs of topical oestrogens?

A

Breast cancer
Angina
VTE

275
Q

What are the CIs of HRT?

A

Breast cancer
Angina
VTE

276
Q

What is Bartholin’s cyst?

A

Bartholin’s glands either side of posterior part of vaginal introitus- Usually pea sized and not palpable
Ducts blocked- Glands swell

277
Q

What is the function of Bartholin’s glands?

A

Produce mucus to help with vaginal lubrication

278
Q

Outline presentation of Bartholin’s cysts

A

Usually unilateral
Swollen, tender
If infected- Bartholin’s abscess- Hot, tender, red, potentially draining pus

279
Q

Outline management of Bartholin’s cyst

A

Usually resolve with good hygiene, analgesia and warm compress
Biopsy if vulval malignancy needs excluding

280
Q

Outline management of Bartholin’s abscess

A

ABs
Swab
E. coli most common cause
Swab for chlamydia and gonorrhoea

Surgery:
Word catheter- Local anaesthetic
Marsupialisation- General anaesthetic

281
Q

What are the complications of lichen sclerosus?

A

5% risk developing SCC of vulva
Pain and discomfort
Sexual dysfunction
Bleeding
Narrowing of vaginal or urethral openings

282
Q

What is Lichen Sclerosus?

A

Chronic inflammatory skin condition
Patches of shiny ‘porcelain-white’ skin
Commonly affects labia, perineum and perianal skin
Associated with AI diseases- T1D, alopecia, hypothyroid and vitiligo

283
Q

How is lichen sclerosus diagnosed?

A

Clinically- History and examination
If doubt- Vulval biopsy

284
Q

What is lichen simplex?

A

Chronic inflammation and irritation caused by repeated scratching and rubbing of an area of skin
Excoriations, plaques, scaling and thickened skin

285
Q

What is lichen planus?

A

AI
Localised inflammation with shiny, purplish, flat-topped raised areas with Wickham’s striae

286
Q

Outline presentation of lichen sclerosus

A

Woman 45-60y
Vulval itching and skin changes in vulva
Soreness and pain possibly worse at night
Skin tightness
Superficial dyspareunia
Erosions
Fissures
Koebner phenomenon

287
Q

What is the Koebner phenomenon?

A

Signs and symptoms made worse by friction to skin

288
Q

Outline appearance of lichen sclerosus

A

Fissures, cracks, erosions, or haemorrhages under skin
Porcelain white
Shiny
Tight
Thin
Slightly raised
May be papules or plaques

289
Q

How is lichen sclerosus managed?

A

Can’t be cured
Follow up every 3-6mths
Potent topical steroids- Clobetasol propionate 0.05% (dermovate)- Reduce risk of malignancy
Emollients

290
Q

What is androgen insensitivity syndrome?

A

Cells unable to respond to androgen hormones due to lack of androgen receptors
X-linked recessive
Extra androgens converted into oestrogen- Female secondary sexual characteristics
Genetically male, female external genitalia
Testes in abdomen, absence of female internal organs

291
Q

What is the role of anti-Mullerian hormone?

A

Produced by testes which prevents female internal organs developing
Shrinks Mullerian ducts

292
Q

Outline presentation of androgen insensitivity syndrome

A

Inguinal hernia containing testes
Primary amenorrhoea
Lack of pubic hair
Lack of facial hair
Male type muscle development
Taller than female average
Infertile
Increased risk testicular cancer

293
Q

Outline hormone test results of androgen insufficiency syndrome

A

Raised LH
Normal/raised FSH
Normal/raised testosterone (for a male)
Raised oestrogen levels (for a male)

294
Q

Outline management of androgen insensitivity syndrome

A

Bilateral orchidectomy to avoid testicular tumours
Oestrogen therapy
Vaginal dilators or vaginal surgery to create adequate vaginal length
Support and counselling

295
Q

Outline vaginal hypoplasia and agenesis

A

Abnormally small vagina/absent vagina
Occur due to failure of Mullerian ducts to develop properly
Ovaries often unaffected- Normal female sex hormones

296
Q

How are vaginal hypoplasia and agenesis managed?

A

Vaginal dilator
Vaginal surgery

297
Q

What is a transverse vaginal septae?

A

Septum forms transversely across vagina- Can be perforate or imperforate
Perforate- Still menstruate but may have difficulty with intercourse/tampon use
Imperforate- Cyclical pelvic symptoms w/o menstruation
Can lead to infertility

298
Q

How is transverse vaginal septae diagnosed?

A

Examination
US
MRI

299
Q

How is transverse vaginal septae managed?

A

Surgical correction- Can cause vaginal stenosis and recurrence

300
Q

What is an imperforate hymen?

A

Hymen at entrance of vagina fully formed, w/o an opening

301
Q

How does imperforate hymen present?

A

Primary amenorrhoea
Cyclical pelvic pain and cramping but no vaginal bleeding

302
Q

How is an imperforate hymen diagnosed and managed?

A

Clinical examination
Surgical incision to create opening

303
Q

What could potentially occur if an imperforate hymen is not treated?

A

Retrograde menstruation leading to endometriosis

304
Q

Outline bicornate uterus

A

2 horns of uterus- Heart shaped
Diagnosed on Pelvis US

305
Q

Outline complications of bicornate uterus

A

Miscarriage
Premature birth
Malpresentation

306
Q

Outline basic embryological development

A

Female: Paramesonephric ducts (Mullerian ducts)- Upper vagina, cervix, uterus, fallopian tubes

Male: Produce Anti-Mullerian hormone- Suppresses growth of Mullerian ducts

307
Q

Outline the types of FGM

A

Type 1: Removal of part or all of clitoris
Type 2: Removal of part or all of clitoris and labia minora, labia majora may also be removed
Type 3: Narrowing or closing of vaginal orifice (infibulation)
Type 4: All other unnecessary procedures to female genitalia

308
Q

List immediate complications of FGM

A

Pain
Bleeding
Infection
Swelling
Urinary retention
Urethral damage and incontinence

309
Q

List long term complications of FGM

A

Vaginal infections- Bacterial vaginosis
Pelvic infections
UTIs
Dysmenorrhoea
Sexual dysfunction and dyspareunia
Infertility
Sig. psych issues and depression
Reduced engagement with healthcare and screening

310
Q

Outline management of FGM

A

Mandatory to report <18y to police
Social services and safeguarding
De-infibulation in cases of type 3
Re-infibulation- Illegal

311
Q
A

Final Year (14 decks)

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