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1
Q

What are the mechanisms of contraception in the COCP

A

inhibit ovulation.

inhibit proliferation of the endometrium, creating unfavourable conditions for implantation

increases the thickness of cervical mucus, preventing passage of sperm.

2
Q

How does the COCP inhibit ovulation

A

negative feedback effect of the oestrogen and progesterone on the hypothalamo-pituitary axis prevents the surge in LH
thus preventing ovulation

3
Q

What is the difference between monophasic and phasic COCP

A

Monophasic pills: every pill contains the same levels of oestrogen and progesterone.

Phasic pills: the level of oestrogen and progesterone in the pills changes throughout the cycle.

4
Q

What are the advantages of the COCP

A

Non-invasive method.
Menses tend to become regular, lighter and less painful.
Running packets together allows control of timing of menses for events such as holidays, exams, and sporting competitions.
improves acne.
It may help symptoms of premenstrual syndrome (PMS).
reduce the risk of ovarian, endometrial and colorectal cancer
It may reduce risk of ovarian cysts.
Normal fertility returns immediately after stopping usage

5
Q

What are the disadvantages of the COCP

A

User-dependent - relies on remembering to take it regularly
Side effects - headaches, breast tenderness and mood changes
increased risk VTE
May cause an increase in blood pressure.
Breakthrough bleeding (BTB) may occur, particularly in the first few months of use.

6
Q

Who should not take the COCP

A

BMI greater than 35
Breast feeding
Smoking >15 per day over the age of 35
Hypertension
History of or family history of venous thromboembolisms
Prolonged immobility due to surgery or disability
Diabetes mellitus with complications e.g. retinopathy
History of migraines with aura
Breast cancer or primary liver tumours
Heart disease - IHD, Valvular or congenital heart disease with complications. Also cardiomyopathy with impaired cardiac function, Atrial fibrillation.

7
Q

What are some side effects of the COCP

A
Breakthrough bleeding. 
Weight gain and Mood changes - but no evidence
breast tenderness, 
headaches
nausea.
8
Q

How is the COCP taken?

A

The COC pill should be started on the first day of menstrual bleeding, but can be started up to day 5 without the need for extra protection.

When started at any other time in the cycle, additional contraceptive precautions (eg, condoms) should be used for seven days

taken for 21 consecutive days, at approximately the same time of day

followed by seven pill-free days (or seven days of neutral tablets) to allow endometrial shedding and a withdrawal bleed. Contraception is still provided during the hormone-free interval.

Explain that only the first pill is taken on the first day of the woman’s period. Future packets will all be started on the same day of the week as the first packet, following a strict 28-day cycle.

9
Q

What counts as a missed COCP?

A

If they take it more than 48 hours after the last pill (ie more than 24 hours late) it counts as a missed pill.

10
Q

What is the advice given for a single missed COCP

A

The last pill missed should be taken now, even if it means taking two pills in one day.
The rest of the pack should be taken as usual.
No additional contraception is needed.
The seven-day break is taken as normal.

11
Q

What is the advice given for two or more missed COCP

A

The last pill missed should be taken now, even if it means taking two pills in one day.
Any earlier missed pills should be left.
The rest of the pack should be taken as usual and additional precautions (eg, condoms or abstinence) should be taken for the next seven days.

If the pills are missed in the first week of a pack (pills 1-7): emergency contraception should be considered if the patient had unprotected sex in the pill-free interval or the first week of the pill packet. She should finish the packet and have the usual pill-free interval.

If the pills are missed in the second week of a pack (pills 8-14): there is no need for emergency contraception as long as the pills in the preceding seven days have been taken correctly. The packet should be finished and the usual pill-free interval taken.

If the pills are missed in the third week of a pack (pills 15-21): the next pack of pills should be started without a break - ie the pill-free interval is omitted. If taking a packet with dummy/placebo pills, these should be discarded, and the new packet started. Emergency contraception is not required.

12
Q

How often should a woman taking the COCP be followed up?

A

After the first prescription, review at 3 months.
If all is well, follow up at 6- to 12-month intervals.
Supplies of up to a year may be issued.

13
Q

How is the COCP managed around the time of surgery?

A

discontinued 4 weeks before elective major surgery
restarted on day one of the next period, occurring at least 2 weeks after mobilisation.

Progestogen-only contraception can be offered as an alternative during this time.

Women requiring emergency surgery should receive subcutaneous heparin and compression stockings.

14
Q

What is the mechanism of action of the POCP

A

thickens the cervical mucus due to the high levels of progesterone. This prevents the entry of sperm and thereby fertilisation of the oocyte.

suppression ovulation (60% of cycles with pills containing levonorgestrel, 97% of cycles with desogestrel)

thinning of the endometrium which inhibits implantation.

15
Q

What are the advantages of the POCP compared to the COCP

A

It is an effective and safe form where oestrogens are contra-indicated

It contains an even lower dose of progestogen than low-dose combined contraceptives and no oestrogen.

It can be used during breast-feeding.

It is suitable for women about to undergo major surgery or surgery on their legs.

There is no evidence that the POCP is associated with an increased risk of VTE

16
Q

What are the disadvantages of the POCP

A

It has to be taken meticulously at the same time each day. (three hours window for traditional, 12 hours in newer with desogestrel)

It is just as susceptible to substances that cause enzyme induction, like rifampicin, many anticonvulsants and St John’s wort.

It does not control the menstrual cycle as effectively as the COCP - causes irregular menstruation or amenorrhoea.

There may be minor side-effects such as breast tenderness, skin changes, and headaches. These usually improve with time.

There is an increased risk of ovarian cysts, perhaps up to 30%.

There may be a small increased risk of breast cancer for women taking the POCP.

17
Q

What are some contraindications to the POCP

A

Past history of breast cancer.
Severe cirrhosis.
Liver tumours.
Stroke and coronary heart disease
Systemic lupus erythematosus (SLE) with positive antiphospholipid antibodies.
Those on medication, including antiretroviral therapy, enzyme-inducing anticonvulsants (but not lamotrigine which is contra-indicated with the COCP), and enzyme-inducing antibiotics such as rifampicin and rifabutin.

18
Q

How should the POCP be started?

A

on the first day of menstruation, giving immediate contraceptive cover

If started any day up to the fifth day from the start of menstruation, no additional contraceptive precautions are required.

If started at any other time in the cycle, pregnancy should be excluded first, and additional contraceptive precautions should be used for 48 hours (eg, condoms or abstinence).

19
Q

What should a woman do if she misses her POCP

A

She should take the missed pill as soon as she remembers and resume her usual pill-taking schedule - even if this means taking two pills on the same day, ie one when she remembers and the next pill on time.

In addition, if the pill is more than three hours late (12 hours for desogestrel pills such as Cerazette®) other contraceptive precautions are required (eg, condoms) or abstinence for the next 48 hours.

Consider emergency contraception if there was unprotected sexual intercourse 2-3 days prior to the missed pills, or there has been intercourse since the missed pill(s).

20
Q

What are the common side effects of POCP

A

Irregular menstrual bleeding patterns

21
Q

Which drugs are liver enzyme inducers and therefore alter the effectiveness of the pill?

A

Anticonvulsants such as carbamazepine, oxcarbazepine, phenytoin, barbiturates, primidone, and topiramate.
NB: Lamotrigine does not affect the POCP.

Antibiotics - rifabutin and rifampicin (potent enzyme inducers).

St John’s wort.

Antiretrovirals - particularly ritonavir-boosted protease inhibitors.

22
Q

How does the IUD work?

A

It releases copper, which makes the uterus an unfavourable environment for sperm.

creates an endometrial inflammatory reaction, inhibiting implantation if fertilisation has already occurred.

23
Q

How soon does the IUD work as a contraceptive?

A

immediately

24
Q

What are the advantages of the IUD

A

Rapid return of fertility post-removal.
Convenience (long-lasting method that is independent of intercourse).
No hormonal content.

25
Q

What are the disadvantages of the IUD

A

heavier and more painful menstruation

discomfort of fitting.

26
Q

What are absolute contraindications to using the IUD

A

Infection
History of pelvic inflammatory disease (PID) or purulent cervicitis in prev 3 months
Recent exposure to sexually transmitted infection (STI).
Septic abortion or postpartum endometritis in the previous 3 months.

Pregnancy
Current pregnancy.
Between 48 hours and 4 weeks postpartum.

Uterine factors
Uterine abnormality distorting the uterine cavity - eg, fibroids, bicornuate uterus.
Uterus less than 5.5 cm in length on sounding. (The device may be expelled, but may also be less effective eg, if placed in one horn of bicornuate uterus)

Gynaecological cancers
Ovarian, cervical or endometrial cancer.
Malignant trophoblastic disease.
Undiagnosed irregular vaginal bleeding/suspicion of genital malignancy.

Adverse reactions to copper
Copper allergy or Wilson’s disease.

Other factors
Previous history of bacterial endocarditis after prosthetic valve replacement.
Significant immunosuppression.

27
Q

What are the side effects of the IUD

A

prolonged, heavier and more painful periods

There is a sixfold increase in risk of PID in the first 20 days following insertion.

Ectopic pregnancy is increased relative to normal pregnancies where copper devices are used.

Failure of insertion

Syncope at insertion

Suspected perforation at insertion

Cramping after insertion

Expulsion

Infection

Lost threads

28
Q

What is the mechanism of action of the IUS

A

suppressant effect on the endometrium, which prevents implantation

There is an increase in endometrial phagocytic cells which also prevents implantation.

Decreased sperm penetration of cervical mucus and impaired sperm migration.

29
Q

What are the advantages of the IUS

A

Rapid return of fertility post-removal.
Reduced menstrual loss and dysmenorrhoea.
Convenience (long-lasting method that is independent of intercourse).
Lack of significant interactions with hepatic enzyme-inducing drugs.
Compared to long-acting injectable depot contraceptives there is no demonstrable effect on bone mineral density (BMD),

30
Q

What are the disadvantages of the IUS

A

Initial menstrual irregularities.

Fitting an IUS is technically more difficult (in view of its larger diameter) than fitting an IUCD, particularly in nulliparous or perimenopausal women.

31
Q

What are the absolute contraindications to using the IUS

A

Infection:
History of pelvic inflammatory disease (PID) or purulent cervicitis in prev 3 months
Recent exposure to sexually transmitted infection.
Septic abortion or postpartum endometritis in the previous three months.

Pregnancy.
Current pregnancy.
Between 48 hours and four weeks postpartum

Uterine factors:
Uterine abnormality distorting the uterine cavity - eg, fibroids, bicornuate uterus. This is mainly due to difficulties with insertion.
Uterus less than 5.5 cm in length on sounding: the device may be expelled, but may also be less effective (eg, if placed in one horn of bicornuate uterus).

Gynaecological cancers:
Ovarian, cervical, breast or endometrial cancer.
Malignant trophoblastic disease.
Undiagnosed irregular vaginal bleeding/suspicion of genital malignancy.

Contra-indications to LNG:
Current deep vein thrombosis (DVT) or pulmonary embolus (PE).
Ischaemic heart disease.
Active viral hepatitis, severe decompensated cirrhosis, benign liver tumours or malignant hepatomas.
Breast cancer within the preceding five years.

Other:
Previous history of bacterial endocarditis after prosthetic valve replacement.
Significant immunosuppression.

32
Q

What are the side effects and complications of the IUS

A

Irregular bleeding and spotting are common in the first six months with an LNG-IUS.

Oligomenorrhoea or amenorrhoea likely if persisting for one year.

Acne, headaches, breast tenderness and nausea are reported by LNG-IUS users but these do not differ significantly from IUCD users.

If a woman does become pregnant with an LNG-IUS in situ, ectopic pregnancy risk is 1 in 20, so she should seek medical advice to exclude it.

There is a six-fold increase in risk of PID in the first 20 days following insertion.

Failure of insertion

Syncope at insertion

Suspected perforation at insertion

Cramping after insertion

Expulsion

Infection

Lost threads

33
Q

What kinds of emergency contraception are there

A

oral progestogen-only emergency contraceptive = levonorgestrel 1.5mg

selective progesterone receptor modulator (SPRM) = ullipristal acetate 30mg

IUD

34
Q

How do the hormonal methods of emergency contraception work

A

delay ovulation for 5-7 days
therefore sperm are no longer viable
no known effect on disruption/inhibition of implantation

35
Q

How does the IUD work as emergency contraception

A

inhibitory effect on both fertilisation and implantation.

Fertilisation inhibition occurs through direct toxicity effects of the copper on both ovum and sperm.

Inflammatory reaction effects on the endometrium due to the Cu-IUCD being in situ can also prevent implantation.

If fertilisation has occurred, the mode of action is by preventing a fertilised egg implanting.

36
Q

What factors should be taken into account when deciding which form of emergency contraception to use?

A

Time since sexual intercourse
Note what contraception was used at the time of intercourse, if any.

Go through menstrual history:
What was the date of the last menstrual period?
Was the last period normal?
What is the usual cycle length?
Is ovulation likely to have taken place yet this cycle?
Could implantation of a fertilised ovum have occurred this cycle?

Note whether there has been any other unprotected intercourse this cycle and whether the woman might already be pregnant.

Establish whether there has been any previous use of EC.

Ask whether the woman is breast-feeding.

Discuss obstetric and gynaecological history (with particular attention to history of pelvic inflammatory disease (PID), current vaginal discharge, history of ectopic pregnancy).

Discuss current requirement for contraception.

Note medications used - eg, enzyme-inducing agents such as phenytoin (ask about over-the-counter enzyme inducers such as St John’s wort).

Take account of general health, looking for any contra-indications - eg, liver disease, porphyria.

Sexual history - consider the risk of sexually transmitted infection (STI).

37
Q

How is the likely date of implantation calculated?

A

Implantation occurs no earlier than five days after ovulation.

To calculate the likely date of implantation, subtract 14 days from the date of the expected date of the next period and add five days

38
Q

When can the hormonal emegency contraceptives be used

A

progestogen - up to 72 hours after intercourse

39
Q

When can the hormonal emergency contraceptives be used

A

progestogen - up to 72 hours after intercourse

ullipristal acetate - up to 120 hours after intercourse

40
Q

What are the contraindications to using the progestogen emergency contraception

A

Hypersensitivity to LNG.
Acute porphyria.
Severe liver disease.
Severe malabsorption syndromes (eg, Crohn’s disease) might impair the efficacy of LNG-EC.
Rare hereditary problems of galactose intolerance

Caution is recommended if there is a history of ectopic pregnancy. Previous ectopic pregnancy is not an absolute contra-indication

41
Q

What are the contraindications to using the ullipristal acetate

A

Pregnancy or suspected pregnancy
Severe liver disease
uncontrolled asthma
Repeated use within the same menstrual cycle

42
Q

When can the IUD be used as emergency contraception

A

Can be used up to five days after sexual intercourse

If the timing of ovulation can be estimated, insertion can be beyond five days after UPSI, as long as insertion does not occur beyond five days from ovulation.

43
Q

What precautions should be taken when inserting an IUD as emergency contraception

A

There is a potential risk of PID when inserting an IUCD in a woman who has had UPSI.

It is recommended that, as a minimum, women at higher risk of STI (age ≤25 years, new sexual partner or ≥1 sexual partner in the previous year) should be offered testing for chlamydia.

For such high-risk women, the use of prophylactic antibiotics should also be considered when the IUCD is inserted.

44
Q

Which contraceptives take 7 days to become effective if not started on first day of period

A

combined oral contraceptive pill
Depo Provera (injectable contraceptive)
intrauterine system (e.g. Mirena)
Nexplanon (implantable contraceptive)

45
Q

Which contraceptives take 2 days to become effective if not started on first day of period

A

progestogen only pill

46
Q

Which method of contraception decreases the risk of endometrial cancer

A

COCP

47
Q

Which method of contraception causes weight gain

A

Depo Provera is the only method of contraception which has a proven link with weight gain.

48
Q

What is the contraception advice post partum?

A

The earliest date of ovulation in a non-breastfeeding woman is thought to be day 28 postpartum.

Therefore, contraception is required from day 21 onwards, as sperm can survive for up to 7 days.

A woman who is exclusively breastfeeding will take longer to ovulate, however, contraception should still be advised if pregnancy is not desired.

The Cu-IUD should not be inserted before day 28 postpartum, due to the increased risk of uterine perforation if inserted before this time.

49
Q

What is an ectopic pregnancy

A

a pregnancy that implants outside the uterine cavity.

50
Q

Where are ectopic pregnancies most common

A

fallopian tubes

most in ampulla. also isthmus or fimbriae

51
Q

What is a heterotropic pregnancy

A

coexistence of both an intrauterine pregnancy and an extrauterine pregnancy

52
Q

What are the risk factors for ectopic pregnancy

A
PID
prev ectopic
IVF
adhesions
IUD/IUS
POCP
smoking
>35y
53
Q

What are the symptoms of an ectopic pregancy

A
severe abdominal/pelvic pain
amenorrhoea, missed period
PV bleed - clots?
dizziness, fainting, syncope
shoulder tip pain
shock
54
Q

What causes shoulder tip pain in an ectopic pregnancy

A

rupture, leakage of blood, irritates diaphragm

55
Q

What are the signs of ectopic pregnancy

A

abdominal or pelvic tendernes
cervical motion tenderness
pallor
tachycardia, low BP

56
Q

Give some differentials for ectopic pregnancy

A
gynae:
miscarriage
molar pregnancy
ruptured ovarian cyst
ovarian torsion
PID

gastro:
constipation
crohn’s
appendicitis

urinary:
UTI
renal colic

57
Q

What investigations should be done in suspected ectopic pregnancy

A

pregnancy test
serum hCG
PV USS

58
Q

What are the options in management of ectopic pregnancy

A

expectant
medical
surgical

59
Q

When is expectant management suitable for ectopic pregnancy

A
unruptured
<30mm 
no heart beat visible
asymptomatic
serum hCG <200 and falling
60
Q

When is medical management suitable for ectopic pregnancy

A

All four requirement fulfilled:

No significant pain.
An unruptured ectopic pregnancy with an adnexal mass smaller than 35 mm with no visible heartbeat.
Serum hCG level less than 1500 IU/L.
No intrauterine pregnancy (as confirmed on an ultrasound scan).

61
Q

When is surgical management suitable for ectopic pregnancy

A

Any of:

Significant pain.
Adnexal mass of 35 mm or larger.
Fetal heartbeat visible on an ultrasound scan.
Serum hCG level of 5000 IU/L or more.

62
Q

Describe the expectant management of ectopic pregnancy

A

monitor serum hCG over 48 hours

if increasing, active management is required

63
Q

Describe the medical management of ectopic pregnancy

A

one off dose of methotrexate

most patients experience abdominal pain 2-3 days after administration of methotrexate.
Other side-effects include nausea, vomiting and reversible impaired liver function.

Women should have blood taken for LFTs and to ensure hCG levels are dropping.

64
Q

Describe the surgical management of ectopic pregnancy

A

laparoscopic salpingectomy or salpingotomy

65
Q

When is a salpingotomy used in the management of ectopic pregnancy

A

if the woman has other risk factors for infertility

66
Q

When do women get a choice between medical and surgical management for ectopic pregnancy

A

serum hCG level of at least 1500 IU/L and less than 5000 IU/L, are able to return for follow up, and meet all of the following criteria:

No significant pain.
An unruptured ectopic pregnancy with an adnexal mass smaller than 35 mm with no visible heartbeat.
No intrauterine pregnancy (as confirmed on an ultrasound scan).

67
Q

What advice is given to women after medical managemet of an ectopic pregnancy

A

use contraception for next 3-6m

risk of teratogenicity of methotrexate to fetus

68
Q

What follow up is needed after management of an ectopic pregnancy

A

serum hCG levels - check they are falling
anti D rhesus prophylaxis if mother rhesus -ve
offer early scan at 6-7 in future pregnancies to establish location and viability

69
Q

What are the potential complications of an ectopic pregnancy

A

tubal rupture, leading to massive haemorrhage, DIC, shock and death
recurrent ectopic pregnancy - 18.5%
psychological - grief, anxiety, depression

70
Q

Define a miscarriage.

What is early/late

A

loss of a pregnancy before 24 weeks

early - <12
late - 13-24

71
Q

What are the risk factors for miscarriage

A

> 30 years, even more common in those aged >35 years
Cigarette smoking
Excess alcohol
Low pre-pregnancy BMI.
Paternal age >45 years (independent of maternal age).
Fertility problems and taking longer to conceive.
Illicit drug use.
Uterine surgery or abnormalities - eg, incompetent cervix.
Connective tissue disorders (systemic lupus erythematosus, antiphospholipid antibodies - lupus anticoagulant/anticardiolipin antibody).
Uncontrolled diabetes mellitus.
Being stressed, anxious or experiencing one or more stressful or traumatic events.

72
Q

What are potential causes of a miscarriage

A

Unknown!

Abnormal fetal development.
Genetically balanced parental translocation.
Uterine abnormality.
Incompetent cervix (second trimester).
Placental failure.
Multiple pregnancy.
Polycystic ovary syndrome.
Antiphospholipid syndrome.
Inherited thrombophilias.
Infections.
Poorly controlled diabetes.
Poorly controlled thyroid disease.
73
Q

What is a threatened miscarriage

A

vaginal bleeding in the presence of a viable pregnancy in the first 24 weeks of gestation.
mild symptoms of bleeding.
Usually little or no pain.
cervical os is closed

74
Q

What is an inevitable miscarriage

A

a diagnosed non-viable pregnancy in which bleeding has begun and the cervical os is open, but pregnancy tissue remains in the uterus.

The pregnancy will not continue and will proceed to incomplete or complete miscarriage.

presents with heavy bleeding with clots and pain.

75
Q

What is an incomplete miscarriage

A

diagnosed non-viable pregnancy in which bleeding has begun but pregnancy tissue remains in the uterus.
previous proof of pregnancy

76
Q

What is a complete miscarriage

A

all the products of conception have been expelled from the uterus and bleeding has stopped.

presents with a history of confirmed intrauterine pregnancy, followed by heavy bleeding and clots but a subsequent ultrasound scan shows no pregnancy tissue in the uterine cavity

77
Q

What is a missed miscarriage

A

diagnosed when a non-viable pregnancy is identified on ultrasound scan, without associated pain and bleeding.

the fetus is dead but retained.
The uterus is small for dates.
A pregnancy test can remain positive for several days or even weeks in some cases.
Early pregnancy symptoms may have decreased or gone.

78
Q

What are the symptoms and signs of miscarriage

A

PV bleed - clots, POC,
haemodynamic instability - dizzy, SOB
cramping suprapubic pain - worse than a period

if fever or rigors - SEPTIC???

79
Q

What should be examined in a potential miscarriage

A

general - signs of haemodynamic instability
abdo - tenderness, distended (?ectopic)
speculum - open or closed os, POC in vaginal canal
bimanual - cervical motion tenderness

80
Q

Give some differentials for miscarriage

A
ectopic pregnancy
cervical malignancy
cervical ectoprion
implantation bleed
endocervical polyp
81
Q

What investigations can be done in miscarriafe

A

TV USS
serum BhCG and again 18 hours later
blood group, Rh status
FBC, CRP and trible vaginal swabs if ?septic

82
Q

How large does the fetus need to be to determine if the pregnancy is viable or not by presence of the fetal heart beat on USS

A

CRL >7mm or gestational sack is >25mm

If the CRL <7.0mm and no fetal heart is identified, a conclusive diagnosis of miscarriage cannot be made – a repeat scan in at least 7 days is required.

83
Q

What can serial hCG measurements tell us about a miscarriage

A

if >63% increase, likely to be ongoing pregnancy

if >50% decrease, pregnancy unlikely to continue

if between, need repeat TV USS

84
Q

What are the management options for miscarriage

A

expectant
medical
surgical

85
Q

Describe expectant management of miscarriage

A

waiting to see if the miscarriage will resolve naturally without intervention with a urine pregnancy test at 7-14 days

86
Q

When should the decision for expectant miscarriage management be reviewed?

A

If bleeding and pain have not started or bleeding and pain are persisting and/or increasing and miscarriage is incomplete or not started

resolution of bleeding and pain with positive pregnancy test after three weeks. Consider either medical or surgical management.

87
Q

Which women should be cautioned against expectant management of miscarriage

A

An increased risk of haemorrhage (for example, she is in the late first trimester).

A previous adverse or traumatic experience associated with pregnancy (such as stillbirth, miscarriage, or antepartum haemorrhage).

An increased risk from the effects of haemorrhage (for example, if she has coagulopathies or is unable to have a blood transfusion).

Any evidence of infection

88
Q

What can be expected from expectant management of miscarriage

A

most of the blood is reabsorbed
there may be loss of products of conception, heavy bleeding and pain
Unpredictable timing

89
Q

What are the advantages of expectant management of miscarriage

A

Can remain at home,
no side effects of medication,
no anaesthetic or surgical risk.

90
Q

What are the risks of expectant management of miscarriage

A

bleeding
chance of being unsuccessful requiring further intervention
need for transfusion.

91
Q

Describe the medical management of miscarriage

A

vaginal misoprostol (prostaglandin analogue) to stimulate cervical ripening and myometrial contractions

give antiemetics and analgesics

92
Q

What are the advantages of medical management of miscarriage

A

Can be at home if patient desires, with 24/7 access to gynaecology services,
avoids anaesthetic and surgical risk.
feel more in control

93
Q

What are the risks of medical management of miscarriage

A

more bleeding and pain than surgical
side effects of medication: vomiting/diarrhoea, heavy bleeding and pain during passage of POC,
chance of requiring emergency surgical intervention.

94
Q

Describe the surgical management of miscarriage

A

manual vacuum aspiration under LA in OPD if <12w

surgical under GA in theatre - a speculum is passed to visualize the cervix, it is dilated allowing suction tube to be passed and remove the products of conception.

95
Q

What are the indications for surgical management of miscarriage

A

persistent excessive bleeding,
haemodynamic instability,
evidence of infected retained tissue
suspected gestational trophoblastic disease.

96
Q

What are the advantages of surgical management of miscarriage

A

rapid resolution of symptoms
Planned procedure (may help patient to cope with miscarriage),
unaware during the process (patient under general anaesthetic).

97
Q

What are the risks of surgical management of miscarriage

A
Anaesthetic risk, 
infection (endometeritis), 
uterine perforation, 
haemorrhage, 
Ashermen’s syndrome, 
cervical tears
bowel or bladder damage, 
retained products of conception.
98
Q

How are women followed up after a miscarriage and what advice is given

A

pregnancy test after 3 weeks
anti D prophylaxis if rh -ve and had surgical management
cancel antenatal appointments

avoid sex until symptoms have resolved
menstruation resumes in 4-8 weeks, so can continue trying if pregnancy is desired and feel able to cope
grief is common - comparable in nature, intensity, and duration to grief reactions in people suffering other types of major loss. Distress is commonly at its worst up to 6 weeks after a miscarriage.

99
Q

Define recurrent miscarriages

A

the occurrence of three or more consecutive pregnancies that end in miscarriage of the fetus before 24 weeks of gestation

100
Q

Give some causes of recurrent miscarriages

A

antiohospholipid syndrome

Parental chromosomal rearrangements – a balanced reciprocal or Robertsonian chromosomal translocation.
Embryonic chromosomal abnormalities

uncontrolled diabetes
uncontrolled thyroid disease
PCOS

Uterine malformations – such as septate, bicornuate or acuate uterus.
Cervical weakness – where the cervix begins to efface and dilate before the pregnancy reaches term
Acquired uterine abnormalities – such adhesions (Asherman’s syndrome) or fibroids.

Inherited thrombophilias - Factor V Leiden, prothrombin gene mutation and deficiencies of protein C/S and antithrombin III.

101
Q

How would cervical weakness leading to miscarriage present?

A

a second-trimester miscarriage

preceded by a spontaneous rupture of membranes or painless cervical dilatation.

102
Q

How would inherited thrombophilias leading to miscarriage present?

A

second trimester pregnancy loss,

the presumed mechanism being thrombosis of the uteroplacental circulation.

103
Q

What investigations can be done in recurrent miscarriage

A

Antiphospholipid antibodies – two positive tests at least 12 weeks apart for either lupus anticoagulant, anticardiolipin antibodies or anti-B2-glycoprotein antibodies.

karyotyping and cytogenetic analysis - parents and products of conception of the third and subsequent consecutive miscarriage

HbA1c, TFT

PV USS - used to assess uterine anatomy.
there is no test for cervical weakness!

Inherited thrombophilia screen – including Factor V Leiden, prothrombin gene mutation and protein S deficiency.

104
Q

How are recurrent miscarriages due to genetic problems managed

A

referred to a clinical geneticist.

Reproductive options will then include proceeding to a further natural pregnancy (with or without a prenatal diagnosis test), gamete donation and adoption.

105
Q

How are recurrent miscarriages due to cervical weakness managed

A

cervical cerclage if:
Previous poor obstetric history (≥3x 2nd trimester losses).
Cervical length shortening on USS (<25mm before 24/40 and a previous 2nd trimester loss).
Symptomatic women with premature cervical dilatation and exposed fetal membranes in the vagina.

if not, serial cervical sonographic surveillance can be offered

106
Q

What are the complications of cervical cerclage

A

bleeding,
membrane rupture,
stimulating uterine contractions

107
Q

How are recurrent miscarriages due to thrombophilias managed

A

Women with second-trimester miscarriage associated with inherited thrombophilias may have an improved live birth rate with heparin therapy during pregnancy.

108
Q

How are recurrent miscarriages due to Antiphospholipid Syndrome managed

A

low-dose aspirin plus heparin

109
Q

What is PMB

A

post menopausal bleeding

vaginal bleeding that occurs after 12 months of amenorrhoea in a woman where the menopause can be expected to have occurred

110
Q

What are the causes of PMB

A

Endometrial cancer UNTIL PROVEN OTHERWISE
Vaginal atrophy - most common cause
Use of HRT.
Endometrial hyperplasia
Endometrial polyps or cervical polyps.
Cervical cancer
Ovarian cancer, especially oestrogen-secreting (theca cell) ovarian tumours.
Vaginal cancer
Vulval cancer
Non-gynaecological causes including trauma or a bleeding disorder.

111
Q

What questions should be asked in a PMB history

A

timing, consistency and quantity of the bleeding,

full gynaecological and obstetric history.

risk factors for endometrial cancer
menstrual timeline from menarche to menopause.

A full drug history including HRT use should be sought.

Red flag symptoms for gynaecological cancer should be enquired about

112
Q

What investigations for PMB need to be done

A

within 2 weeks:

TVUS - if endometrial thickness >4mm then:

hysteroscopy
endometrial biopsy for histology

113
Q

What kind of cancer is endometrial cancer

A

most are adenocarcinoma

oestrogen-dependent endometrioid (type 1)
oestrogen-independent non-endometrioid carcinomas (type 2).

114
Q

What are the risk factors for endometrial cancer

A
Being nulliparous 
Menopause past the age of 52.
Obesity
Endometrial hyperplasia (associated with the presence of concomitant endometrial cancer.)
HNPCC
Polycystic ovary syndrome
Diabetes mellitus
Tamoxifen 
HRT
115
Q

What investigations need to be done for endometrial cancer

A

TV USS
hysteroscopy
biopsy

116
Q

State the staging of endometrial cancer

A

IA confined to endometrium with no, or less than half, myometrium invaded.
IB invasion equal to, or more than half of, myometrium.

II - invasion into the cervical stroma but it has not extended outside the uterus.

Stage IIIA - invasion of serosa or adnexa or positive peritoneal cytology and possibly more than one of these.
Stage IIIB - vaginal or para-metrial metastases.
Stage IIIC - metastases to pelvic (IIIC1) or para-aortic (IIIC2) lymph nodes, or both.

Stage IVA - involvement of bowel or bladder mucosa.
Stage IVB - distant metastases including nodes in the abdomen or inguinal region.

117
Q

What is the management for stage I endometrial cancer

A

hysterectomy and BSO

can give progestogen in stage 1A if fertility is a concern

118
Q

What is the management for stage II endometrial cancer

A

radical hysterectomy and pelvic node clearance

119
Q

What is the management for stage III or IV endometrial cancer

A

debulking surgery if good performance status and tumour is resectable

chemo/rad if suitable

120
Q

What is endometrial hyperplasia

A

abnormal proliferation of endometrium - more than the normal proliferation during a menstrual cycle

121
Q

What are the types of endometrial hyperplasia

A

hyperplasia without atypia

atypical hyperplasia - this is pre-malignant

122
Q

What are the risk factors for endometrial hyperplasia

A
obesity 
Exogenous oestrogen use (without cyclical progesterone)
Oestrogen-secreting ovarian tumour.
Tamoxifen use
Polycystic ovarian syndrome (due to anovulation).
Nulliparity.
HNPCC
Diabetes.
123
Q

What is a protective factor for endometrial cancer and hyperplasia

A

COCP

124
Q

Why does obesity increase the risk of trial cancer and hyperplasia

A

androgens are converted to oestrogen within adipose tissue

unopposed oestrogen

125
Q

What effect does tamoxifen use have on the risk of gynae cancers

A

reduces risk breast cancer

increases risk endometrial cancer

126
Q

What are some symptoms of endometrial hyperplasia

A
post menopausal bleed
intermenstrual bleed
irregular bleed
menorrhagia
vaginal discharge
127
Q

What investigations are needed for endometrial hyperplasia

A

TV USS
hysteroscopy
endometrial biopsy

128
Q

What is the management of endometrial hyperplasia without atypia

A

Reassurance: risk of progression to cancer is less than 5% over 20 years a
Address any risk factors
Follow-up biopsies
Progestogen treatment for at least 6m: IUS is the first-line option. The second-line option is continuous oral progestogen treatment

Hysterectomy in some cases

129
Q

How often should a woman with endometrial hyperplasia without atypia have repeat biopsies?

A

six-monthly until two consecutive biopsies have been negative.
Annual biopsy thereafter should be considered in women at higher risk (eg, BMI ≥35),

130
Q

When might a hysterectomy be considered for a woman with endometrial hyperplasia without atypia

A

Regression has not occurred despite a year of progestogen treatment.
There is change to atypical hyperplasia.
There is relapse after treatment.
The woman wishes to have surgery rather than long-term medical treatment and regular biopsy.

131
Q

What is the management of atypical endometrial hyperplasia

A

Total hysterectomy - due to the risk of malignant progression, with bilateral salpingo-oophorectomy in addition for postmenopausal women.

For women who wish to preserve fertility:
progestogen - IUS, oral
regular monitoring by three-monthly endometrial biopsy,
have a hysterectomy as soon as potential fertility is no longer required.

132
Q

What should a women with atypical endometrial hyperplasia be advised about pregnancy

A

wait until regression on medical treatment has occurred (at least one negative biopsy).

133
Q

Define infertility

A

failure to conceive after frequent unprotected sex for one or two years

134
Q

What is the difference between primary and secondary infertility

A

primary - the couple have never conceived before

secondary - have managed to conceive before

135
Q

What is subfertility

A

any form of reduced fertility that results in an prolonged duration of unwanted lack of conception

136
Q

What percentage of couples will conceive within 1 year, 2 years and 3 years

A

84% of couples in the general population will conceive naturally within 1 year if they have regular (every 2–3 days) unprotected sexual intercourse.

92% after 2 years
93% after 3 years

137
Q

In how many couples is there no identifiable cause for their infertility

A

25%

138
Q

What are the groups of causes for female infertility

A
ovulation disorder
tubal, uterine end cervical disorders
drugs
age
stress
lifestyle
139
Q

Which ovulation disorders can cause infertility

A

Group I ovulation disorders - hypothalamic pituitary failure - low gonadotrophins and oestrogen deficiency.

Group II ovulation disorders are defined as dysfunctions of the hypothalamic-pituitary ovarian axis - PCOS and hyperprolactinaemic amenorrhoea.

Group III ovulation disorders are caused by ovarian failure and are characterized by high gonadotrophins and hypogonadism and a low oestrogen level.

Thyroid abnormalities

Adrenal abnormalities — Cushing’s syndrome and congenital adrenal hyperplasia .

Chronic debilitating disease (such as uncontrolled diabetes, cancer, AIDS, end-stage kidney disease, and malabsorption)

140
Q

Which tubal, uterine and cervical factors can lead to infertility

A
STI
PID
sterilisation
endometriosis
cervical mucus defect
submucosal fibroids
cervical or pelvic surgery
141
Q

Whcih drugs can lead to infertility

A
NSAIDs and COX inhibitors
Spironolactone
Chemotherapy with cytotoxic drugs
Neuroleptic drugs
Contraceptives 
Recreational drugs such as marijuana and cocaine
142
Q

How long does it take for fertility to return to normal after using contraceptives

A

immediately: COCP, POP, LUNG-IUS Cu-IUD

few months: combined contraceptive patch and the combined vaginal ring

up to 1 year: the progestogen-only injectables

143
Q

What questions should you ask in a woman presenting with infertility

A
any prev pregnancies or miscarriages
freq/problems with intercourse
contraception - type and use
menstrual history- heacy, infequent, amenorrhoea
history of PID or endometriosis
STIs
pelvic surgery
any systemic disease
drugs
occupation
lifestyle - drugs, alcohol, smoking, obesity
144
Q

What might you want to examine in a female presenting with infertility

A

BMI
hirsutism, acne - PCOS
abdo - ovarian cyst
pelvic - vaginismus, endometriosis, PID, fibroids

145
Q

What investigations can be done in infertility

A
mid-luteal phase progesterone - taken 7 days before period
chlmaydia screen
FSH and LH 
TFT
prolactin
hysterosalpingography - tubal factors
diagnostic laparoscopy
146
Q

How can infertility be managed

A

general:
reduce stress, stop smoking, healthy BMI, reduce alcohol, check drugs

medical:
induce ovulation - clomifene

surgical:
tubal microsurgery
ablation or resection of endometriosis
correction of epidymal blockage

assisted conception;
IUI
IVF
intracytoplasmic sperm injection
donor insemination
oocyte donation
embryodonation
147
Q

What are the risks involved in assisted conception techniques

A

ovarian hyperstimulation syndrome
ectopic pregnancy
pelvic infection
multiple pregnancy

148
Q

What are the symptoms of ovarian hyperstimulation syndrome

A

Mild - abdominal bloating and mild abdominal pain.
Moderate — nausea and vomiting and increased abdominal discomfort.
Severe — oliguria, generalized oedema, abdominal pain and/or distension (caused by enlarged ovaries and acute ascites), and hydrothorax (occasionally).
Critical — oligo/anuria, tense ascites or large hydrothorax, thromboembolism, and acute respiratory distress syndrome.

149
Q

What does the mid luteal phase progesterone result show

A

whether ovulation is occurring or not

>30 indicates ovulation

150
Q

What is menorrhagia

A

excessive menstrual blood loss that occurs regularly (every 24 to 35 days) which interferes with a woman’s physical, emotional, social, and material quality of life.

151
Q

How can menorrhagia be defined quantitatively

A

> =80 mL
a duration of more than 7 days
the need to change menstrual products every one to two hours,
passage of clots greater than 2.54 cm

152
Q

What are some causes of menorrhagia

A
DUB - iagnosis o exclusio
fibroids
endometriosis
adenomyosis
PID
endometrial cancer
endometrial hyperplasia
PCOS
coagulaopathy - von willebrand's disease
hypothyroid
obesity
DM
liver or renal disease
iatrogenic - anticoagulation, chemotheraphy, IUD
153
Q

What questions should be asked in the history of a patient with menorrhagia

A
menstrual - length cycle, duration period, how many towels/tampons, clots, LMP (?pregnancy)
PCB
IMB
dysparuenia
dysmenorrhoea
vaginal discharge
impact on life
symptoms of anaemia

cervical screening
obstetric history
contraception
sexual history

PMH - hypothyroid, diabetes, kidney, liver, PCOS
DH
FH - endometriosis, coagulation

154
Q

What examination should be done in a patient with menorrhagia

A

general - thyroid, PCOS, bruising, anaemia
abdo
pelvic
speculum

155
Q

What investigations should be done in menorrhagia

A

FBC, TFT, coag,
USS
vaginal swabs

156
Q

What is the management of menorrhagia if there is no underlying pathology

A

LNG-IUS
tranexaminc acid during menses
NSAID - mefanamic acid (if dysmenorrhoea)
COCP
noresthisterone day 5-26, or depo-provera

157
Q

What is adenomyosis

A

endometrial tissue in the myometrium

can be due to uterine damage eg. pregnancy, c-section, uterine surgery, surgical management of miscarriage or TOP

158
Q

What is an adenomyoma

A

collection of endometrial glands forming a grossly visible nodule

159
Q

What are the features of adenomyoma

A

menorrhagia
dysmenorrhoea - progressive
deep dyspareunia
irregular bleeding

160
Q

How is adenomyosis investigated

A

TV US

161
Q

How is adenomysosi managed

A
NSAIDs
COCP, POP, IUS, aromatase inhibitors
ablation
uterine artery embolisation
hysterectomy
162
Q

What is endometriosis

A

presence of tissue resembling endometrial glands and stroma outside teh uterien cavity
induce chronic inflammatory reaction, leading to adhesions
most deposits are in the pelvis

163
Q

What can endometriosis in the ovaries cause

A

endometriotic ovarian cysts (endometriomas)
containing blood and endometriosis-like tissue may develop,
which may rupture

164
Q

What are symptoms of endometriosis

A

cyclical pelvic pain (cam become constant if adhesions)
dysmenorrhoea
dyspareunia
menorrhagia

dysuria
dyschezia (defecation)
subfertility

165
Q

What is seen on examination in endometriosus

A
enlarged ovaries
adnexal masses
pelvic tenderness
fixed retroverted uterus
nodules on uterosacral ligaments or in pouch of Douglas
166
Q

How is endometriosis investigated

A

TV US

laparoscopy - gold standard

167
Q

What is seen on laparoscopy in endometriosis

A

chocolate cysts
adhesions
peritoneal endometrial deposits

168
Q

How is endometriosis managed

A

NSAIDs
supressing ovulation (leads to regression of depositis) - COPC, mirena, depo-provera
surgery - excision, laser ablation. hyserectomy

169
Q

What are fibroids

A

leiomyoma
benign tumour - mixture of smooth muscle cells and fibroblasts
hard, round whorled tumour in the myometrium

170
Q

What controls the development and maintenance of fibroids

A

oestrogen and progesterone

171
Q

What is the differnce between subserosal, intramural and submucosal fibroids in terms of location and symptoms

A

Subserosal fibroids — near outer serosal surface of the uterus and extend into the peritoneal cavity. Asymptomatic cause symptoms due to pressure on adjacent structure

Intramural fibroids — within the myometrium without extending predominately into the uterine cavity or peritoneal cavity. Can cause menorrhagia and dysmenorrhea by interfering with the constriction of blood vessels during menstruation.

Submucosal fibroids — near the inner mucosal surface of the uterus, extend into the uterine cavity. Cause significant menorrhagia and dysmenorrhea or reduce fertility.

172
Q

Which type of fibroids are most common

A

intramural

173
Q

What are the risk factors for fibroids

A
age
early puberty
obesity
black, asian
FH
174
Q

How are fibroids felt on examination

A

firm, enlarged irregularly shaped mass in a non-tender uterus

175
Q

How are fibroids investigated

A

TV US

176
Q

How are fibroids managed

A
tranexamic or mefanamic acid
COCP, POP, IUD
transcervical resection of fibroid
myomectomy - if want to preserve uterus
uterine artery embolisation
hysterectomy
177
Q

What drugs can be pescribed priro o surgery for uterine fibroids? Why?

A

GnRH analogues eg. zolidex
- suppress ovulation so decrease ssize of fibroids and reduce risk of complications

selective progesterone receptor modulators eg. ullipristal acetate
- decrease fibroid size if <3cm and reduce menorrhagia

178
Q

What is PCOS

A

heterogenous endocrine disorder
hyperandogenism
high LH leads to androgen production by ovaries, anovulation
insulin resistance

179
Q

How does insulin resistance increase androgen production in PCOS

A

insulin resistance leads to increased insulin secretion
the liver then produces less serum hormone binding globulin
leads to more free androgens

180
Q

What are the features of PCOS

A
oligomenorrheoa
hirsutism
acne
anovulation
polycystic ovaries
181
Q

What are the symptoms of PCOS

A
oligo/amenorrhoea
infertlity
hirsutism
obesity
chronic pelvic pain
depression
182
Q

What can be seen on examination in PCOS

A

hirsutism
acanthosis nigracans
male pattern hair loss

183
Q

What are the criteria for diagnosis of PCOS

A

Rotterdam criteria - need 2/3

oligomenorrhoea or anovulation
hyperandrogenism - clinical or biochemical
Polycysitc ovaries on imaging

184
Q

What investigations are need in PCOS

A

testosterone, serum hormone binding globulin, LH/FSH, progesterone, TFT, prolactin, OGTT
TV USS

185
Q

What are the expected blood test results in PCOS

A

high LH
high testosterone
low progesterone
low serum hormone binding globulin

186
Q

Hwo is PCOS managed

A

if amenorrhoea - COCP to induce endometrial bleeds
weight loss - BMI <30 reduces symptoms
if infertility - clomifene +- metformin
for hirsutism - antiandrogen meds

187
Q

What is amenorrhoea

A

absence or cessation of menses

188
Q

What is the differnce between primary and secondary amenorrheoa

A

Primary amenorrhoea = failure to establish menstruation by 16 years of age in women and girls with normal secondary sexual characteristics, or by 14 years of age in women and girls with no secondary sexual characteristics

Secondary amenorrhoea =t he absence of menstruation for at least 6 months in women with previously normal and regular menses, or for 12 months in women with previous oligomenorrhoea

189
Q

What is oligomenorrheoa

A

menses occurring less frequently than every 35 days

190
Q

What are the hypothalmic causes of amenorrhoea

A

due to low GnRH

functional - eating disorders, exercise

Kallman syndrome - X linked failur eof migration of GnRH producing cells

191
Q

What are the pituitary causes of amenorrhoea

A

prolactinomas - raised prolactin leads to inhibition of GnRH
pituitary tumours - mass effect
Sheehan’s syndrome - post partum necrosis
post contraception

192
Q

What are the ovarian causes of amenorrhoea

A

PCOS
Turner’s
premature ovarian failure

193
Q

What are the key blood test results in premature ovarian failure

A

high FSH

low oestrogen

194
Q

What are the adrenal causes of amenorrhoea

A

adrenal hyperplasia

195
Q

What are the structural causes of amenorrhoea

A

Asherman’s syndrome - intrauterine adhesions

transverse vaginal septum

196
Q

What are the systemic causes of amenorrhoea

A

perimenopause
thyroid disease
diabetes
meds - antipsychotics/antiepileptics

197
Q

How should amenorrhoea be investigated

A

pregnancy test!!!
TFT, FSH, LH, oestrodiol, progesterone, testosterone, prolactin
TV US
karyotyping

198
Q

How is premature ovarian failure treated

A

cyclical hormone replacement therapy with oestrogen

reduces risk of cardiovascular disease, osteoporosis and symptoms of menopause