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James' Phase 3A Medicine > Obstetrics and Gynaecology > Flashcards

Obstetrics and Gynaecology Flashcards

1
Q

Name 3 hormones that are important in pregnancy.

A

Main hormones:

  1. hCG.
  2. Progestins.
  3. Oestrogens.

Other hormones:

  1. hPL.
  2. Prolactin.
  3. Oxytocin.
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2
Q

Where is hCG produced?

A

The trophoblast.

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3
Q

Give 2 functions of hCG.

A
  1. It signals the presence of the blastocyst.

2. It prevents the corpus luteum from dying - luteal regression.

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4
Q

Where are progestins produced?

A

Initially from the corpus luteum and then from the placenta from week 7.

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5
Q

Give 3 functions of progestins.

A
  1. Prepares the endometrium for implantation.
  2. Promotes myometrial quiescence.
  3. Increases maternal ventilation.
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6
Q

How do progestins prepare the endometrium for implantation?

A

Progestins stimulate the proliferation of cells, vascularisation and the differentiation of endometrial stroma.

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7
Q

Where are oestrogens produced?

A

Initially in the ovary and then from a combination of fetal and maternal sources.

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8
Q

Give 2 functions of oestrogens in pregnancy.

A
  1. Promotes a change in the CV system.

2. Alters carbohydrate metabolism.

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9
Q

What is the main oestrogen in pregnancy?

A

E3 - it indicates fetal well-being.

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10
Q

What is the role of E2 in pregnancy?

A

E2 is responsible for proliferation of the endometrial epithelium. It also facilitates progesterone action.

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11
Q

What is the role of human placental lactogen (hPL)?

A
  1. Mobilises glucose from fat.
  2. Acts as an insulin antagonist.
  3. Converts mammary glands into milk secreting tissues.
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12
Q

What is the role of prolactin?

A

Prolactin is responsible for milk production.

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13
Q

What is the role of oxytocin?

A

Oxytocin is responsible for milk secretion and uterine contractions.

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14
Q

Where is prolactin produced?

A

In the anterior pituitary gland.

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15
Q

Where is oxytocin produced?

A

In the posterior pituitary gland.

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16
Q

Where are FSH and LH produced?

A

In the anterior pituitary gland.

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17
Q

What hormone does the hypothalamus release that acts on the anterior pituitary gland and stimulates the production of FSH and LH?

A

GnRH.

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18
Q

What cells in the ovaries does FSH act on?

A

Granulosa cells -> oestrogen production.

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19
Q

What cells in the ovaries does LH act on?

A

Theca cells -> androgen production.

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20
Q

What hormone is released from the hypothalamus that acts on the anterior pituitary to inhibit prolactin release?

A

Dopamine.

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21
Q

What is the principle foetal nutrient?

A

Glucose.

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22
Q

Can the foetus produce any of its own glucose?

A

No, gluconeogenic enzymes are inactived in the foetus and so all its glucose has to come from its mother.

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23
Q

In early pregnancy, is plasma glucose high or low?

A

Plasma glucose is lower because glucose is being stored.

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24
Q

Why is plasma glucose lower in early pregnancy?

A

Because the mother is storing glucose.

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25
Q

In late pregnancy, is plasma glucose high or low?

A

Plasma glucose is higher. This is due to maternal insulin resistance and glucose sparing for the foetus.

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26
Q

Why is plasma glucose higher in late pregnancy?

A
  1. Because of increasing maternal insulin resistance.

2. Glucose sparing for the foetus.

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27
Q

What are the consequences of maternal insulin resistance?

A

Maternal insulin resistance -> gestational diabetes -> increased risk of macrosomia and shoulder dystocia.

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28
Q

Why is the immune response suppressed in a pregnant lady?

A

It prevents foetal rejection.

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29
Q

Give 4 ways in which foetal rejection is prevented in a pregnant lady.

A
  1. A TH2 bias is observed.
  2. Syncytiotrophoblast has no self:non-self markers and so doesn’t stimulate an immune response.
  3. Extra-villous trophoblast cells have modified markers.
  4. The overall immune response is suppressed.
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30
Q

In a normal pregnancy, a TH2 bias is observed, this helps prevent foetal rejection. Give 3 potential consequences if there is not a TH2 bias.

A
  1. Pre-eclampsia.
  2. IUGR.
  3. Miscarriage.
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31
Q

How does the endometrial epithelium become adhesive to the blastocyst?

A

The blastocyst and endometrium communicate via the release of hormones -> ‘sticky endometrium’.

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32
Q

When in a woman’s cycle does the endometrium become sticky?

A

This usually happens between days 20-24. This is called the window of implantation and outside of this time implantation will not occur.

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33
Q

What reaction occurs when a blastocyst implants into the endometrium?

A

A primary decidual reaction occurs.

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34
Q

What part of the blastocyst facilitates placental formation?

A

The cytotrophoblast.

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35
Q

Placenta formation: What does the cytotrophoblast go on to form?

A

Anchoring villi -> extra villous trophoblast.

Floating villi are also involved.

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36
Q

What can trigger the differentiation of anchoring villi into extra-villous trophoblast?

A

Hypoxia.

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37
Q

What is the role of extra villous trophoblast (EVT) cells?

A

EVT invade and remodel spiral arteries. This leads to more hypoxia and so more EVT; a positive feedback effect is observed.

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38
Q

Why do EVT cells invade and remodel spiral arteries?

A

To allow for optimum nutrient delivery for the baby.

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39
Q

Give 3 potential consequences of poor endovascular remodelling.

A
  1. Pre-eclampsia.
  2. IUGR.
  3. Pre-term birth.
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40
Q

Where should normal placenta invade into?

A

The decidua.

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41
Q

What is placental accreta?

A

When the placenta invades into the superficial myometrium.

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42
Q

What is placental increta?

A

When the placenta invades into the deeper myometrium.

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43
Q

What is placental percreta?

A

Invasion of the placenta into nearby organs e.g. the bladder.

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44
Q

What are the potential consequences, if left untreated, of a rhesus negative mother having a rhesus positive foetus?

A

There is a risk of RBC lysis -> foetal anaemia and death.

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45
Q

Describe the pathophysiology of rhesus disease.

A
  1. Foetal Rh+ RBC’s leak through the placenta and interact with the mother’s blood -> IgM reaction -> sensitisation.
  2. IgM can’t cross the placenta and so there is no RBC lysis but memory B cells are created.
  3. On a subsequent pregnancy, IgG may cross the placenta and cause foetal RBC lysis.
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46
Q

What is the only antibody that can cross the placenta?

A

IgG.

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47
Q

How can foetal RBC lysis be prevented in rhesus negative mothers?

A

Anti-D prophylaxis can be given. This destroys Rh+ IgG and so no RBC are attacked.

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48
Q

What is quiescence?

A

When the myometrium is inactive, there are no contractions.

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49
Q

Describe the physiology behind quiescence?

A

Increased cAMP -> K+ extrusion -> myocyte hyperpolarisation -> muscle fibres are unable to contract.

There is also phosphorylation of intracellular proteins -> actin-myosin ATPase is inactivated -> smooth muscle relaxation.

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50
Q

Give 2 theories behind the induction of labour.

A
  1. Placental clock theory.

2. Signals from the baby.

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51
Q

Induction of labour: describe the placental clock theory.

A

Increased release of CRH from the placenta -> foetal ACTH release -> release of oestrogens, formation of myometrial gap junctions -> regular and co-ordinated uterine contractions.

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52
Q

Induction of labour: describe the theory that suggests that there are signals from the baby.

A

Increased ACTH or increased foetal surfactant proteins activate amniotic fluid macrophages. These migrate to the uterine wall, there is up-regulation of inflammatory gene expression which stimulates labour.

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53
Q

Describe the 3 stages of parturition.

A
  1. Dilation - cervical remodelling and uterine contractions.
  2. Expulsion - full dilation to delivery of infant.
  3. Placental delivery.
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54
Q

Parturition: do progesterone levels fall when the cervix dilates and remodels?

A

Progesterone levels don’t fall but it becomes ineffective -> contractions.

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55
Q

Parturition: what happens in the expulsion phase that triggers myometrial contractions?

A

Oxytocin release -> increased intracellular Ca2+ -> myometrial contractions.

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56
Q

Why can nifedipine be used to inhibit premature contractions?

A

Nifedipine is a CCB and so can block the rise of intracellular calcium therefore inhibiting muscle contraction.

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57
Q

Name 2 drugs that can inhibit uterine contractions.

A
  1. Nifedipine - CCB.

2. Atosiban - oxytocin antagonist.

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58
Q

Name an oxytocin analogue that can indue labour.

A

Syntocinon.

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59
Q

Why is the incidence of breast cancer thought to be increasing?

A
  1. Western lifestyle.
  2. Screening.
  3. Increasing life expectancy.
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60
Q

What percentage of women who have a mammogram will be called back for more tests?

A

4/100 will need more tests.

1/4 of these women will then be found to have cancer.

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61
Q

Breast cancer: what is the triple assessment?

A
  1. Clinical examination e.g. palpation.
  2. Mammogram.
  3. Core needle biopsy.
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62
Q

Breast cancer: is a P1/2 lump that is described as soft, mobile and regular likely to be benign or malignant?

A

Benign. E.g. fibroadenoma.

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63
Q

Breast cancer: is a P4/5 lump that is described as hard, fixed and irregular likely to be benign or malignant?

A

Malignant.

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64
Q

Name 3 modifiable RF’s for breast cancer.

A
  1. Alcohol intake.
  2. Obesity.
  3. Use of HRT/OCP.
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65
Q

Name 3 non-modifiable RF’s for breast cancer.

A
  1. Age of menarche/menopause.
  2. Breast density.
  3. Genetics e.g. BRCA1/2.
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66
Q

Approximately what percentage of breast cancers are ductal and what percentage are lobular?

A
  • Ductal (70%).

- Lobular (10%).

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67
Q

Give 4 signs that you may find on clinical examination that are suggestive of breast cancer.

A
  1. Palpable lump - irregular, hard, fixed, painless.
  2. Discharge from the nipple.
  3. Nipple in-drawing.
  4. Skin changes e.g. peau d’orange.
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68
Q

If a patient has breast implants or high density breasts a mammogram can be difficult to interpret. What investigation can be done as an alternative?

A

An MRI.

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69
Q

Give 3 treatment options for patients with breast cancer.

A
  1. Conservative surgery + radiotherapy.
  2. Mastectomy + radiotherapy.
  3. Mastectomy + reconstruction + radiotherapy (BUT can damage a lot of reconstructions).
  4. Axillary lymph node removal - limited removal or clearance.
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70
Q

Why might a mastectomy be indicated as opposed to a lumpectomy in someone with breast cancer?

A
  1. If the tumour is large relative to the size of breast.
  2. If there are multiple tumours.
  3. Patient preference.
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71
Q

What biopsy should you do to ensure that breast cancer hasn’t spread to the axillary lymph nodes?

A

A sentinel node biopsy.

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72
Q

Name 2 adjuvant treatments that can be given to women with oestrogen receptor + cancer.

A
  1. Tamoxifen (pre-menopausal).

2. Aromatase inhibitors (post-menopausal).

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73
Q

Why might a woman with breast cancer have chemotherapy?

A

If she has a very aggressive cancer or to shrink a tumour prior to surgery.

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74
Q

Give 3 non-pharmacological therapies that can be used to help manage labour pain.

A
  1. Trained support.
  2. Acupuncture.
  3. Hypnotherapy.
  4. Massage.
  5. Hydrotherapy.
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75
Q

Give 5 pharmacological therapies that can be used to help manage labour pain.

A
  1. Gas and air - entonox.
  2. Paracetamol.
  3. Codeine.
  4. Opioids e.g. pethidine, diamorphine.
  5. Epidural.
  6. Spinal anaesthesia.
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76
Q

Give 3 potential side effects of opioids.

A
  1. Sedation.
  2. Respiratory depression.
  3. Nausea and vomiting.
  4. They cross the placenta readily.
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77
Q

Where is spinal anaesthesia injected into?

A

The CSF.

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78
Q

Name an anaesthetic that can be given as an epidural.

A

Bupivacaine.

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79
Q

How does Bupivacaine work as an epidural?

A

It blocks sodium channels.

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80
Q

Give 3 indications for an epidural.

A
  1. Maternal request.
  2. Augmented labour.
  3. Twins.
  4. Existing co-morbidities.
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81
Q

Give 3 contraindications for an epidural.

A
  1. Maternal refusal.
  2. Local infection.
  3. Allergy.
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82
Q

Why would a general anaesthetic be given for performing a c-section?

A

If there is a threat to the mum or the foetus and so a regional anaesthetic is contraindicated.

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83
Q

Give 2 disadvantages of using a general anaesthetic for a c-section.

A
  1. Risk of aspiration.

2. Given IV and so the baby is anaesthetised too.

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84
Q

Give 3 advantages of using local anaesthetic when performing a c-section.

A
  1. Safer.
  2. You can see the baby immediately.
  3. Partner present.
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85
Q

Give 3 disadvantages of using local anaesthetic when performing a c-section.

A
  1. It can cause hypotension.
  2. It can cause headaches.
  3. The patient may experience discomfort from pressure sensations.
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86
Q

Define miscarriage.

A

The loss of a pregnancy before 24 weeks of gestation.

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87
Q

In approximately what percentage of pregnancies does miscarriage occur?

A

20%.

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88
Q

What is a threatened miscarriage?

A

When a lady experiences bleeding +/- pain but the cervical os is closed.

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89
Q

What is an inevitable miscarriage?

A

When a lady experiences heavy bleeding, clots, pain and the cervical os is open.

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90
Q

Define complete miscarriage.

A

When all the products of conception leave the body.

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91
Q

Define recurrent miscarriage.

A

> 3 consecutive miscarriages.

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92
Q

Give 4 potential causes of miscarriage.

A
  1. Abnormal foetal development.
  2. Uterine abnormality.
  3. Incompetent cervix.
  4. Placental failure.
  5. Multiple pregnancy.
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93
Q

Give 3 risk factors for miscarriage.

A
  1. Age >30.
  2. Smoking.
  3. Excessive alcohol consumption.
  4. Uterine surgery.
  5. Poorly controlled diabetes.
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94
Q

What investigations might you do to determine whether someone has had a miscarriage?

A
  1. Transvaginal USS.

2. Serum hCG.

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95
Q

Describe the management of a miscarriage.

A
  1. Vaginal misoprostol.
  2. Manual vacuum aspiration.
  3. Counselling and support.
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96
Q

What is a molar pregnancy?

A

A molar pregnancy is a type of GTD. It occurs when there is an abnormality in chromosomal number during fertilisation. A non-viable fertilised egg implants and fails to come to term. It grows into a mass in the uterus.

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97
Q

What is gestational trophoblastic disease (GTD)?

A

GTD describes a group of pregnancy related tumours. These tumours can be pre-malignant and often benign e.g. molar pregnancies or malignant e.g. choriocarcinoma and invasive mole.

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98
Q

Describe a partial molar pregnancy.

A

Where an ovum is fertilised by two sperm -> produces cells with 69 chromosomes (triploidy).

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99
Q

Describe a complete molar pregnancy.

A

Where one ovum without any chromosomes is fertilised by one sperm which duplicates. There are 46 chromosomes all of paternal origin.

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100
Q

Which type of molar pregnancy results in 46 chromosomes all of paternal origin?

A

A complete molar pregnancy.

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101
Q

Give 3 risk factor’s for GTD.

A
  1. Maternal age <16 or >45.
  2. Multiple pregnancy.
  3. Previous GTD.
  4. OCP.
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102
Q

Give 3 symptoms of molar pregnancies.

A
  1. Vaginal bleeding in early pregnancy.
  2. Abdominal pain in early pregnancy.
  3. Hyperemesis and hyperthyroidism in late pregnancy due to high levels of B-hCG.
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103
Q

What investigations might you do in someone to determine if they have GTD?

A
  1. Urine and blood B-hCG - will be very high.

2. USS - complete mole has ‘snow storm’ appearance.

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104
Q

What is the treatment for molar pregnancies?

A

Suction curettage.

Chemotherapy.

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105
Q

What is hyperemesis gravidarum?

A

Excessive vomiting, dehydration and ketosis in pregnancy.

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106
Q

With which placental hormone is hyperemesis gravidarum associated?

A

B-hCG.

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107
Q

How is hyperemesis gravidarum managed?

A

Rehydrate with IV fluids, vitamins and frequent small meals.

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108
Q

Give 2 methods used for monitoring the foetal heart rate.

A
  1. Intermittent auscultation using a pinard stethoscope or a hand held doppler.
  2. Continuous monitoring: cardiotocography (CTG).
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109
Q

FHR monitoring: give 2 advantages of intermittent auscultation.

A
  1. Cheap.
  2. Easy to do.
  3. Non invasive.
  4. Can be done at home.
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110
Q

FHR monitoring: give 2 disadvantages of intermittent auscultation.

A
  1. Variability is not detected.
  2. Long term monitoring is not possible.
  3. Quality of FHR can be affected by the maternal HR.
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111
Q

FHR monitoring: give 2 advantages of continuous monitoring.

A
  1. Gives lots of information e.g. variability, accelerations, decelerations etc.
  2. Continuous.
  3. Monitors FHR and uterine contractions.
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112
Q

FHR monitoring: give 2 disadvantages of continuous monitoring.

A
  1. Not very mobile - the mum’s abdomen is strapped.

2. Expensive.

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113
Q

CTG: what is a normal baseline HR?

A

110-160 bpm.

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114
Q

CTG: what is a non-reassuring baseline HR?

A

100-109 bpm.

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115
Q

CTG: what is an abnormal baseline HR?

A

<100 bpm.

>180 bpm.

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116
Q

CTG: what is normal variability?

A

> 5

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117
Q

CTG: what is non-reassuring variability?

A

<5 for 40-90 minutes.

Reduced variability could be due to foetal sleeping.

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118
Q

CTG: what is abnormal variability?

A

<5 for >90 minutes.

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119
Q

CTG: what is an acceleration?

A

An increase in the baseline HR by 10-15 bpm.

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120
Q

CTG: are accelerations reassuring or non-reassuring?

A

The presence of accelerations is reassuring.

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121
Q

CTG: are decelerations reassuring or non-reassuring?

A

Decelerations are non-reassuring.

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122
Q

CTG: what are early decelerations?

A

Early decelerations are seen just before a uterine contraction. They may be due to foetal head compression.

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123
Q

CTG: what are late decelerations?

A

Late decelerations are seen just after uterine contraction. They may be due to placental insufficiency and are often more sinister.

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124
Q

CTG: are early or late decelerations more concerning?

A

Late decelerations are more concerning.

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125
Q

CTG: what are variable decelerations?

A

When there is a mixture of early and late decelerations.

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126
Q

CTG: how would you determine if a CTG was overall normal, suspicious or abnormal?

A
  • Normal: everything is normal and accelerations are present.
  • Suspicious: one non-reassuring feature.
  • Abnormal: >2 non-reassuring features and/or >1 abnormal feature.
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127
Q

How do you define a normal CTG? (BraVAD)

A
  1. Baseline HR - 110-160 bpm.
  2. Variability >5.
  3. Accelerations present.
  4. No decelerations.
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128
Q

What are the parameters used in determining whether a CTG is normal or abnormal?

A
  1. Baseline HR.
  2. Variability.
  3. Accelerations.
  4. Decelerations.
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129
Q

What is the gold standard method for direct FHR monitoring?

A

Scalp ECG.

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130
Q

Give a disadvantage of a scalp ECG for monitoring the FHR.

A
  1. Invasive.
  2. Membranes need to be broken and so cervix must be >2cm.
  3. Risk of scalp injury and infection risk.
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131
Q

What is the role of p53?

A

p53 is a tumour suppressor gene. It is a transcription factor that regulates cell division and death.

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132
Q

What is the role of Rb?

A

Rb is a tumour suppressor gene. It alters the activity of transcription factors and so controls cell division.

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133
Q

If there is a mutation in either p53 or Rb what might happen?

A

If a mutation occurs in these genes a patient may have uncontrolled cell growth -> cancer.

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134
Q

What are the roles of oncogenes?

A

Oncogenes stimulate excessive cell growth and cell division -> cancer development.

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135
Q

Give an example of an oncogene.

A

HER2.

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136
Q

What is the most common type of gynaecological cancer?

A

Endometrial cancer.

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137
Q

What is the pathophysiology behind endometrial cancer?

A

Unopposed oestrogen leads to endometrial hyperplasia and so an increased risk of endometrial adenocarcinoma.

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138
Q

Give 5 risk factors for developing endometrial cancer.

A
  1. Obesity.
  2. Diabetes.
  3. Nulliparity.
  4. Late menopause.
  5. HRT.
  6. Pelvic irradiation.
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139
Q

What is the most common type of endometrial cancer?

A

Endometrial adenocarcinoma.

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140
Q

What is the red flag symptom for endometrial cancer?

A

Post menopausal bleeding!

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141
Q

What investigations might you do if you suspect that a patient may have endometrial cancer?

A
  1. Pelvic and abdominal examination.
  2. Transvaginal USS.
  3. Endometrial biopsy.
  4. Hysteroscopy.
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142
Q

What type of staging is used for endometrial cancer?

A

FIGO staging.

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143
Q

Describe the treatment for endometrial cancer.

A
  1. Hysterectomy +/- pelvic lymph node removal.

2. Adjuvant radiotherapy and progesterone therapy.

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144
Q

Define adenocarcinoma.

A

A malignant tumour of glandular epithelium.

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145
Q

Why is the incidence of cervical cancer decreasing?

A
  1. Screening - cervical smears.

2. HPV vaccine.

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146
Q

Name 2 oncoproteins associated with HPV.

A
  1. E6 - blocks p53.

2. E7 - blocks Rb.

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147
Q

HPV: Which oncoprotein blocks p53?

A

E6.

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148
Q

HPV: Which oncoprotein blocks Rb?

A

E7.

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149
Q

Give 5 risk factors for HPV and so cervical cancer.

A
  1. Early age intercourse (<16).
  2. Multiple sexual partners.
  3. STI’s.
  4. Smoking.
  5. Multiparity.
  6. OCP.
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150
Q

What is the most common type of cervical cancer?

A

Squamous (90%).

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151
Q

What type of staging is used for cervical cancer?

A

FIGO staging.

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152
Q

What is the red flag symptom for cervical cancer?

A

Post-coital bleeding.

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153
Q

Describe the treatment for cervical cancer.

A
  1. <2cm - loop removal, just removing part of the uterus.
  2. > 2cm - radical hysterectomy.
  3. > 4cm - radiotherapy, chemotherapy, palliative care.
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154
Q

What must you consider when treating cervical cancer?

A

Fertility - is the patient likely to want children in the future?

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155
Q

Give 3 potential risks of performing a radical hysterectomy.

A
  1. Bowel problems.
  2. Sexual problems.
  3. Bladder problems.
  4. Lymphoedema.
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156
Q

Describe the aetiology of vulval cancer.

A

Vulval intraepithelial neoplasia (VIN - skin disease). Abnormal cells develop in the surface layers of the skin covering the vulva. It is not vulval cancer but may turn into cancer - pre-malignant. Usual type is associated with HPV infection.

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157
Q

What is the most common type of vulval cancer?

A

Squamous.

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158
Q

Give 5 symptoms of vulval cancer.

A
  1. Itching.
  2. Soreness.
  3. Lump.
  4. Bleeding.
  5. Pain on micturition.
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159
Q

Describe the treatment for vulval cancer.

A
  1. Surgery - radical or conservative.
  2. Radiotherapy.
  3. Chemotherapy.
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160
Q

Give 4 risk factors for developing ovarian cancer?

A
  1. Early menarche.
  2. Late menopause.
  3. Nulliparity.
  4. Genetics e.g. BRCA1/2.
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161
Q

Describe the epidemiology of ovarian cancer.

A

More common in women >50; post-menopausal. Often people present late and so it is advanced at presentation.

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162
Q

What are the commonest types of ovarian cancer?

A
  1. Epithelial (85%).
  2. Sex cord.
  3. Germ cell.
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163
Q

Give 5 symptoms of ovarian cancer.

A
  1. Bloating.
  2. Abdominal pain.
  3. Change in bowel habit.
  4. Urinary frequency.
  5. Bowel obstruction.
  6. Can often be asymptomatic.
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164
Q

What investigations might you do in a patient who you suspect has cervical cancer?

A
  1. Measure CA125.
  2. Trans-vaginal USS.
  3. Calculate the RMI (risk of malignancy index) - if this is >250 the patient should be referred under the 2 week wait system.
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165
Q

How is cervical cancer treated?

A

Surgery and chemotherapy should be offered.

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166
Q

Define incontinence.

A

The involuntary leakage of urine.

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167
Q

Incontinence: What is OAB?

A

Over-active bladder.

There are involuntary detrusor contractions -> urgency.

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168
Q

Give 3 symptoms of OAB.

A
  1. Urgency.
  2. Frequency.
  3. Nocturia.
  4. ‘Key in door’ urgency.
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169
Q

What is stress incontinence?

A

Stress incontinence occurs in patients with a week urethral sphincter. Anything that increases intra-abdominal pressure e.g. coughing, laughing, exercise results in the leakage of urine.

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170
Q

If a patient has a good bladder capacity and small volume leakage would this be more in keeping with a diagnosis of OAB or stress incontinence?

A

Stress incontinence.

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171
Q

What is the functional bladder capacity?

A

400ml.

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172
Q

Describe the epithelium of the detrusor muscle.

A

Smooth muscle with transitional epithelium.

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173
Q

Describe the innervation of the detrusor muscle.

A

Sacral parasympathetic innervation.

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174
Q

What investigations might you do in a patient complaining of incontinence?

A
  1. Bladder diary (frequency volume chart).
  2. Urinalysis.
  3. Residual urine measurement e.g. catheter or USS.
  4. ePAQ.
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175
Q

What information can you obtain from a bladder diary?

A
  1. Frequency.
  2. Quantity of urine.
  3. Fluid intake.
  4. Diurnal variation.
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176
Q

Investigating incontinence: what is ePAQ?

A

A questionnaire regarding urinary, bowel, vaginal and sexual symptoms.

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177
Q

Describe the non-pharmacological treatments for managing OAB.

A
  1. Lifestyle changes e.g. weight loss, stop smoking, reduce caffeine, avoid straining.
  2. Bladder drill.
  3. Pads.
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178
Q

Describe the non-pharmacological treatments for managing stress incontinence.

A
  1. Lifestyle changes e.g. weight loss, stop smoking, reduce caffeine, avoid straining.
  2. Physiotherapy e.g. pelvic floor exercises.
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179
Q

How do pelvic floor exercises work in treating someone with stress incontinence?

A

Pelvic floor muscle contraction -> urethra compression -> increased urethral pressure -> reduced leakage.

Vaginal cones can also be used.

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180
Q

What surgical options can be offered to patients with stress incontinence?

A
  1. Sling.

2. Suspension - restores pressure to the urethra and supports the urethra.

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181
Q

Name 3 drugs that can be used to treat OAB.

A
  1. Oxybutynin.
  2. Mirabegron.
  3. Botulinum Toxin.
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182
Q

How does oxybutynin work in treating OAB?

A

Oxybutynin is anticholinergic, it is an M2/3 receptor antagonist. It works by reducing detrusor muscle innervation and so its activity.

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183
Q

Give 3 potential side effects of oxybutynin.

A
  1. Dry mouth.
  2. Constipation.
  3. Blurred vision.
  4. Cognitive impairment.
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184
Q

How does mirabegron work in treating OAB?

A

It is beta 3 agonist. It relaxes the detrusor muscle and increases bladder capacity.

185
Q

How does botulinum toxin work in treating OAB?

A

It blocks ACh release and so reduces destrusor muscle contraction.

186
Q

Give 3 symptoms of prolapse.

A
  1. Pain.
  2. Lump.
  3. Discomfort.
  4. Sexual symptoms.
187
Q

Describe the management for a patient presenting with a prolapse.

A
  1. Reassurance.
  2. Symptom management.
  3. Vaginal pessaries e.g. ring.
  4. Surgery can be offered if symptoms are severe.
188
Q

Is the detrusor muscle relaxed or contracted during storage?

A

Relaxed.

189
Q

Is the detrusor muscle relaxed or contracted during voiding?

A

Contracted.

190
Q

Describe the physiology of micturition.

A

The bladder fills and stretch receptors are stimulated. Afferent impulses stimulate the parasympathetic action of detrusor muscle; it contracts. The urethral sphincters relax; this is mediated by inhibition of the neurones to them. The PAG is stimulated.

191
Q

How does the COCP work as a contraceptive?

A

The COCP prevents ovulation and alters the cervical mucus, it also thins the endometrium.

192
Q

Give 5 advantages of the COCP as a contraceptive.

A
  1. Reversible.
  2. Reliable.
  3. Regular cycle.
  4. Reduces menorrhagia.
  5. Helps with acne.
  6. Reduces post-menopausal symptoms.
  7. Protective against some kinds of cancer.
193
Q

Give 3 disadvantages of the COCP as a contraceptive.

A
  1. No protection against STI’s.
  2. Drug interactions.
  3. Increased risk of breast and cervical cancer.
  4. VTE risk.
194
Q

How does the POP work as a contraceptive?

A

It thickens the cervical mucus and thins the endometrium.

195
Q

Give 2 advantages of the POP as a contraceptive.

A
  1. Prevents oestrogenic side effects e.g. breast tenderness.

2. Suitable for smokers; those with obesity; those at increased risk of VTE etc.

196
Q

Give 3 disadvantages of the POP as a contraceptive.

A
  1. Less effective than the COCP.
  2. Increased risk of ectopic pregnancy.
  3. Disrupts menstrual pattern.
  4. Functional ovarian cysts may development.
197
Q

What are the Fraser guidelines?

A

A doctor can proceed to give contraceptive advice and treatment to someone <16 provided he is satisfied in the following criteria:

  1. The patient will understand his advice.
  2. The doctor cannot persuade the patient to inform their parents.
  3. The patient is very likely to continue having sexual intercourse with or without contraception.
  4. If the patient does not receive contraceptive advice their physical/mental health will suffer.
  5. It is in the patients best interests to receive contraceptive advice and treatment without parental consent.
198
Q

Why is contact tracing important with regards to sexually transmitted infections?

A
  1. Prevents re-infection.
  2. Breaks the chain of infection.
  3. Allows treatment of asymptomatic individuals.
199
Q

Give 5 questions that are important to ask when taking a sexual health history.

A
  1. When was last intercourse?
  2. Regular/casual partners?
  3. Male/female partners?
  4. Contraceptive use?
  5. Type of intercourse?
  6. How many partners in the last 3 months and 12 months?
200
Q

Give 5 symptoms of STI’s that are seen in women.

A
  1. Abnormal discharge.
  2. Itching.
  3. Soreness.
  4. Ulcers and lumps.
  5. Post intercourse bleeding.
201
Q

Give 5 symptoms of STI’s that are seen in men.

A
  1. Pain on micturition.
  2. Urethral pain.
  3. Abnormal discharge.
  4. Ulcers and blisters.
  5. Swelling.
202
Q

What are the Wilson and Jungner screening criteria?

A
  1. The condition should be a serious health problem.
  2. The natural history of the condition should be understood.
  3. There should be a detectable early stage.
  4. There should be a treatment available.
  5. Facilities for diagnosis and treatment should be available.
  6. There should be a suitable test.
  7. The test should be acceptable to the population.
  8. There should be an agreed policy on whom to treat.
  9. The cost of testing should be balanced against the benefits.
  10. Screening should be a continuous process not just a one off.
203
Q

Define screening.

A

The process of identifying apparently healthy individuals who may be at increased risk of developing a disease.

204
Q

Antenatal care: When would a woman have her booking appointment and what is the purpose of it?

A

8-10w.
Offer general lifestyle advice.
Comprehensive obstetric history and examination.
Check for HIV, Hep.B, Syphillis, Rubella.

205
Q

Antenatal screening: what diseases are being screened for in the foetal anomaly screening test?

A
  1. Down’s (T21).
  2. Edward’s (T18).
  3. Patau’s (T13).
206
Q

Antenatal screening: when should a foetal anomaly screening test be done?

A

A blood sample should be taken by 14+1 weeks.

An anomaly scan is done between 18-20+6 weeks.

207
Q

Antenatal screening: what is the threshold for further testing following a foetal anomaly screening test?

A

If the risk is >1 in 150 then further testing will be done e.g. chorionic villous sample (CVS) or amniocentesis.
NIPT is available privately.

208
Q

When is the dating scan done?

A

An early USS is done at 10-14w, this is used for dating the pregnancy, confirming viability and checking for multiple pregnancy.

209
Q

Antenatal screening: what diseases are being screened for in the infectious diseases screening test?

A
  1. HIV - identify and treat mum and reduce the risk of transmission to the baby.
  2. Hep B - look if mum is infected.
  3. Syphillis - treat mum to prevent congenital syphillis.
210
Q

Describe the inheritance pattern of sickle cell and thalassaemia.

A

Autosomal recessive.

211
Q

Name 3 neonatal screening programmes.

A
  1. New born blood spot.
  2. Hearing test.
  3. New born and 6-8w physical examination.
212
Q

Neonatal screening: what is the new born blood spot?

A

The new born blood spot screens for 9 conditions. A heal prick blood test is done at days 5-8 and looks for CF, congenital hypothyroidism, sickle cell and 6x metabolic diseases e.g. MCADD, phenylketonuria, maple syrup disease etc.

213
Q

Neonatal screening: when is a hearing test done?

A

Within 4 weeks. You are looking for a response in the cochlea.

214
Q

Neonatal screening: when is a new born physical examination done?

A

Within 72 hours of birth. It is repeated at 6-8 weeks by a GP.

215
Q

Neonatal screening: give 4 things that a new born physical examination is looking for.

A
  1. Eye problems.
  2. Heart defects.
  3. Dysplasia of the hips.
  4. Undescended testes.
216
Q

What should a doctor tell a patient in order for the patient to give fully informed consent?

A
  1. The nature of the procedure.
  2. About any reasonable alternatives.
  3. Relevant risks, benefits and uncertainties.
  4. The patient’s understanding should also be assessed.
217
Q

What 4 questions can be asked to assess mental capacity?

A
  1. Does the patient understand the information?
  2. Can the patient retain the information?
  3. Can they use the information to weight up options and make a decision?
  4. Can they communicate their decision?
218
Q

Until what week can a lady legally have an abortion?

A

Abortion is legal in the UK up to 24 weeks under the Abortion Act 1967. After that, it is illegal unless there is a substantial risk to the woman’s life or foetal abnormalities.

219
Q

Define pre-eclampsia.

A

Gestational hypertension which affects the kidneys -> proteinuria (>0.3g protein/24h).

220
Q

Define chronic hypertension.

A

A patient with high BP which is diagnosed prior to pregnancy or before week 20 of pregnancy. Their high BP is not resolved postpartum.

221
Q

Define gestational hypertension.

A

New high BP after 20w gestation and resolves after giving birth. There is no proteinuria.

222
Q

What is eclampsia?

A

Pre-eclampsia (gestational hypertension + proteinuria) and generalised tonic clonic seizures.

223
Q

What medication can be given to women with gestational hypertension/pre-eclampsia?

A

Labetalol or nifedipine.

If no response, delivering the baby will normalise BP.

224
Q

Describe the treatment for eclampsia.

A
  1. Give IV MgSO4 (neuroprotection).
  2. Treat HTN e.g. labetalol.
  3. Stabilise mum.
  4. Deliver baby.
225
Q

Give 5 risk factors for developing eclampsia.

A
  1. Very young or very old mothers.
  2. First pregnancy.
  3. Afro-caribbean ladies.
  4. Multiple pregnancy e.g. twins.
  5. Renal disease.
  6. Existing HTN.
226
Q

Briefly describe the pathophysiology behind pre-eclampsia.

A

Spiral arteries do not remodel -> arteries are tight leading to increased resistance in the placenta -> placental ischaemia -> RAAS activated -> poor renal perfusion, HTN, proteinuria and oedema -> pre-eclampsia.

227
Q

Give 3 signs of pre-eclampsia that are detected at the kidneys.

A
  1. GFR and renal blood flow decrease.
  2. Raised uric acid.
  3. Proteinuria.
228
Q

Give 5 symptoms of pre-eclampsia.

A
  1. Visual change e.g. blurred vision.
  2. Headaches.
  3. Epigastric pain.
  4. Weight gain.
  5. Vomiting.
229
Q

Give 5 signs of pre-eclampsia.

A
  1. Raised BP.
  2. Proteinuria.
  3. Retinal vasospasm.
  4. RUQ tenderness.
  5. Ankle clonus and brisk reflexes.
  6. Pulmonary oedema.
230
Q

Describe the management of pre-eclampsia.

A
  1. Prevent eclampsia and other complications.
  2. Treat raised BP with labetalol or nifedipine.

If there is progressive deterioration in liver or renal function then you should deliver the baby.

231
Q

Define prematurity.

A

Prematurity or preterm is defined as babies born alive before 37 weeks of pregnancy are completed.

232
Q

What organs are most likely to be affected in babies that are born premature and why?

A

The lungs and brain are most likely to be affected as these develop in the 3rd trimester.

233
Q

What is pre-term labour?

A

When there is persistent uterine activity and cervical dilation and/or effacement before 37 weeks.

234
Q

Name 5 things that you can give to a premature baby to improve their survival.

A
  1. Steroids.
  2. Surfactant.
  3. Ventilation.
  4. Antibiotics.
  5. Nutrition.
235
Q

Give 5 risk factors for having a premature baby.

A
  1. Previous pre-term birth.
  2. Vaginal bleeding.
  3. Multiple pregnancy e.g. twins.
  4. Ethnic group.
  5. Genital infections.
236
Q

Define puerperium.

A

The period from placental delivery to 6w after birth - the post-natal period.

237
Q

Give 2 endocrine changes that occur during puerperium.

A
  1. Reduced placental hormones.

2. Increase in prolactin for lactation.

238
Q

Give 3 physiological changes that occur during puerperium.

A
  1. Involution of the uterus.
  2. Decidua sheds as lochia.
  3. Lactation.
239
Q

Puerperium: briefly describe the physiology behind involution of the uterus.

A

There is muscle ischaemia, autolysis and phagocytosis -> involution of the uterus.

240
Q

The decidua sheds as lochia, what are the three stages of this process called?

A
  1. Lochia rubra.
  2. Lochia serosa.
  3. Lochia alba.
241
Q

What is the name of the breast milk that is produced at birth?

A

Colostrum.

242
Q

What does colostrum contain?

A
  • Protein rich.
  • Vitamin A.
  • NaCl.
  • GF’s.
  • Antibodies.
  • Lactoferrin.
243
Q

Briefly describe the physiology of lactation.

A

Baby suckles -> nipples send impulses to brain -> prolactin is released from the ant.pituitary -> milk is produced by lactocytes -> oxytocin is released from the post.pituitary -> myoepithelial contraction -> milk ejection.

244
Q

Name 3 minor things that women are at risk of during puerperium.

A
  1. Infection.
  2. Haemorrhage.
  3. Fatigue.
  4. Anaemia.
  5. Back pain.
  6. Haemorrhoids.
245
Q

Name 3 major things that women are at risk of during puerperium.

A
  1. Sepsis.
  2. Sever haemorrhage.
  3. Pre-eclampsia.
  4. VTE.
  5. Prolapse.
  6. Incontinence.
  7. Depression.
246
Q

Name 3 members of a post-natal MDT.

A
  1. Midwives.
  2. Breastfeeding support workers.
  3. Doula.
  4. Nurses.

If complex, obstetricians and paediatricians will be involved too.

247
Q

Give 3 risk factors for sepsis in pregnancy.

A
  1. Obesity.
  2. Anaemia.
  3. Diabetes.
  4. Amniocentesis/invasive procedures.
248
Q

What can cause sepsis in pregnancy?

A
  1. Endometritis.
  2. Skin infections.
  3. Pyelonephritis.
  4. Chorioamnionitis.
  5. Pneumonia.
249
Q

Define PPH.

A

Post-partum haemorrhage: >500ml estimated blood loss after birth of baby.

250
Q

Define major PPH.

A

> 1500ml blood loss and continuing to bleed/signs of shock.

251
Q

Give 5 risk factors for VTE in pregnancy.

A
  1. Increasing gestational age.
  2. Obesity.
  3. Smoking.
  4. C-section.
  5. Family history.
  6. Immobility.
  7. Multiple pregnancy e.g. twins.
  8. Previous VTE.
252
Q

When is a woman at the greatest risk of VTE?

A

The risk is greatest just after giving birth, in the post partum period.

253
Q

What medication can be given postnatally to reduce a woman’s risk of VTE?

A

LMWH.

TED stockings.

254
Q

Describe the physiology behind a post dural puncture headache?

A

Accidental dural puncture -> CSF leakage and decreased pressure in fluid around the brain.

255
Q

Give 3 symptoms of a post dural puncture headache.

A
  1. Headache is worse on sitting/standing.
  2. Neck stiffness.
  3. Photophobia.
256
Q

How would you treat a post dural puncture headache?

A
  1. Lying flat.
  2. Analgesia.
  3. IV fluids.
257
Q

Give 3 risk factors for urinary retention postnatally.

A
  1. If the woman had an epidural.
  2. Prolonged 2nd stage of labour.
  3. Forceps/ventouse delivery.
258
Q

Give 3 red flag signs that a mother may be developing mental health problems postnatally.

A
  1. Recent change in mental state.
  2. Thoughts/acts of self harm.
  3. Estrangement from the infant.
259
Q

Give 3 symptoms of post-natal depression.

A
  1. Depression.
  2. Irritable.
  3. Tired.
  4. Sleepless.
  5. Appetite change.
  6. Anxious.
  7. Negative thoughts.
260
Q

Define maternal death.

A

The death of a woman while pregnant or within 42 days of termination of pregnancy, irrespective of the duration and the site of the pregnancy, from any cause related to the pregnancy or its management but not accidental causes.

261
Q

What are the 3 most common causes of maternal death?

A
  1. VTE.
  2. Haemorrhage.
  3. Pre-eclampsia.
262
Q

Define menstruation.

A

Monthly bleeding from the reproductive tract due to hormonal changes.

263
Q

What hormone is responsible for thickening the endometrium?

A

Oestrogen.

264
Q

What hormone is responsible for thinning the endometrium?

A

Progesterone.

265
Q

A surge in which hormone leads to ovulation?

A

LH.

266
Q

Approximately how much blood is lost in menstruation?

A

60-80ml.

267
Q

Define menorrhagia.

A

Heavy menstrual bleeding (subjectively considered heavy by the woman) that interferes with physical, emotional and social QOL.

268
Q

Give 3 causes of menorrhagia.

A
  1. Fibroids/polyps.
  2. Coagulation problems.
  3. Endometriosis/adenomyosis.
  4. Hypothyroidism.
  5. Infection.
  6. Ovulatory problems.
  7. Endometrial dysfunction.
269
Q

Give 5 questions that you should ask when taking a history from a lady who is presenting with menorrhagia.

A
  1. How much blood?
  2. How many pads is the lady using? Flooding?
  3. Any clots?
  4. Duration of bleeding?
  5. Any pain?
  6. Impact on ADL’s and QOL?
  7. Any associated symptoms e.g. thyroid? Clotting? Drugs (Warfarin)?
270
Q

What investigations might you do on a lady who is presenting with menorrhagia?

A
  1. FBC, B12/Folate/Iron, TSH, STI screen.
  2. Smear if due.
  3. Transvaginal USS.
271
Q

Describe the management of menorrhagia.

A
  1. Mirena Coil.
  2. Anti-fibrinolytics e.g. tranexamic acid.
  3. NSAIDS.
  4. Progestogens.
  5. COCP.
  6. Endometrial ablation.
  7. Hysterectomy.
272
Q

Name 3 foetal emergencies.

A
  1. Foetal distress.
  2. Cord prolapse.
  3. Shoulder dystocia.
273
Q

Name 3 disorders that are specific to pregnancy.

A
  1. Gestational diabetes.
  2. Pre-eclampsia/eclampsia.
  3. Obstetric cholestasis.
  4. Acute fatty liver in pregnancy.
274
Q

Name 3 disorders that are exacerbated by pregnancy.

A
  1. Hypertension.
  2. Renal disease.
  3. Cardiac disease.
  4. Endocrine disease.
275
Q

Define antepartum haemorrhage.

A

Bleeding from anywhere in the genital tract after 24w gestation.

276
Q

Give 3 causes of antepartum haemorrhage.

A
  1. Placenta praevia/LLP.
  2. Placental accreta.
  3. Placental abruption.
  4. Uterine rupture.
277
Q

Give 3 potential complications of antepartum haemorrhage.

A
  1. Premature labour.
  2. Need for a blood transfusion.
  3. Tubular necrosis.
  4. DIC.
278
Q

When might a LLP be detected?

A

On the 20w anomaly scan. The placenta must be >25mm from the cervical os.

279
Q

Would a woman with a LLP complain of pain?

A

No, a LLP is classically painless.

280
Q

How should a LLP be managed?

A
  1. Advise mum on the symptoms to look out for.
  2. Seek early advice.
  3. If recurrent bleeds, admit until delivery.
  4. Elective c-section at 38 weeks.
281
Q

What is vasa praevia and what are its risks?

A

Vasa praevia is when the foetal vessels lie near the cervical os. There is a risk of damage/rupture to foetal vessels -> foetal distress and haemorrhage.

282
Q

Define placental abruption.

A

Premature separation of the placenta from the uterine wall.

283
Q

How might the uterus feel on physical examination in a woman with placental abruption?

A

The woman may have a ‘woody-hard’ and tense uterus.

284
Q

Give 2 potential consequences of placental abruption.

A
  1. Foetal distress.

2. Maternal shock.

285
Q

Give 5 risk factors for placental abruption.

A
  1. Increasing BMI.
  2. Smoking.
  3. Previous abruption.
  4. Hypertension.
  5. Uterine overdistension e.g. multiple pregnancy.
  6. Trauma e.g. RTA.
  7. Domestic abuse.
286
Q

Define primary PPH.

A

> 500ml blood loss within 24h of delivery.

287
Q

Define secondary PPH.

A

> 500ml blood loss between 24h to 12w post delivery.

288
Q

What can cause PPH?

A

The 4 T’s:

  1. Tissue - is the placenta complete?
  2. Tone - is the uterus contracted?
  3. Trauma - check for tears and repair.
  4. Thrombin - check clotting.
289
Q

Give 5 risk factors for PPH.

A
  1. Large babies.
  2. Nulliparity.
  3. Multiple pregnancy.
  4. Prolonged labour.
  5. Previous PPH.
290
Q

What is cord prolapse?

A

When the cord is presenting -> membrane rupture -> vasospasm.

291
Q

Give a potential consequence of cord prolapse.

A

Hypoxia -> foetal morbidity and mortality.

292
Q

Give 5 risk factors for cord prolapse.

A
  1. Premature rupture of membranes.
  2. Polyhydramnios.
  3. Long cord.
  4. Multiparity.
293
Q

How can cord prolapse be managed?

A
  1. Infuse fluid into the bladder (elevated presenting part of cord).
  2. Trendelenburg position.
  3. Constant monitoring.
  4. Transfer to theatre for delivery.
294
Q

What is shoulder dystocia?

A

Failure of the anterior shoulder to pass under the pubic symphysis after delivery of the foetal head. It requires specific manoeuvres to facilitate delivery.

295
Q

Give 3 risk factors for shoulder dystocia.

A
  1. Macrosomia.
  2. Maternal diabetes.
  3. Post-maturity.
  4. Obesity.
  5. Prolonged labour.
296
Q

How should shoulder dystocia be managed?

A

HELPERR:

H - call for Help.
E - evaluate for Episiotomy.
L - Legs in McRoberts.
P - suprapubic Pressure.
E - Enter pelvis.
R - Rotational manoeuvres.
R - Remove posterior arm.
297
Q

Shoulder dystocia: give 3 potential complications that the mother is at risk of.

A
  1. Vaginal tear.
  2. PPH.
  3. PTSD.
  4. Bladder/uterine rupture.
298
Q

Shoulder dystocia: give 3 potential complications that the baby is at risk of.

A
  1. Cerebral palsy.
  2. Hypoxia.
  3. Brachial plexus injury.
  4. Fractured humerus/clavicle.
299
Q

Give 5 causes of infertility.

A
  1. Ovulatory (25%).
  2. Tubal (20%).
  3. Uterine/peritoneal (10%).
  4. Male factors (30%).
  5. Unexplained (25%).
300
Q

When would you refer a couple for infertility investigations?

A

You refer them for investigations after 1 year of trying to conceive.

301
Q

What would make you consider early referral for investigating infertility?

A

Early referral if the woman is >35, has a menstrual disorder, previous surgery or previous PID/STI and/or if the man has genital pathology, previous STI, systemic illness or an abnormal genital examination.

302
Q

What pre-conception advice would you give to a couple?

A
  1. Have intercourse 2-3 times a week.
  2. Folic acid.
  3. Ensure smears are up to date.
  4. Smoking cessation and reduce alcohol intake.
  5. Manage co-morbidities.
  6. Ensure healthy weight.
303
Q

Name 3 reproductive disorders that are associated with obesity.

A
  1. PCOS.
  2. Miscarriage.
  3. Infertility.
  4. Obstetric complications.
304
Q

What 3 things are investigated in initial infertility tests?

A
  1. Ovulation.
  2. Semen quality.
  3. Tubal patency.
305
Q

Infertility investigations: what initial tests would the GP do?

A
  1. Hormone profile (D2, FSH, D21 progesterone).
  2. TFT’s.
  3. Rubella.
  4. Smear.
  5. Semen analysis.
306
Q

Infertility investigations: how can you check ovulation?

A

Measure mid-luteal progesterone.

307
Q

Infertility investigations: what hormone levels are looked at in order to test ovarian reserve?

A
  1. FSH.
  2. AMH

AFC (antral follicle count) is also determined through imaging.

308
Q

A sperm count less than what will indicate the need for clinical examination and further tests?

A

<5m/ml.

Further testing may include endocrine tests and karyotyping e.g. klinefelters.

309
Q

Infertility investigations: how can tubal patency be investigated?

A
  1. HSG (hysterosalpingogram) imaging.
  2. HyCoSy (Hysterosalpingo-contrast-sonography).
  3. Laparoscopy.
310
Q

How can infertility be managed if there is a mild abnormality?

A

Intrauterine insemination.

311
Q

How can infertility be managed if there is a moderate abnormality?

A

IVF.

312
Q

How can infertility be managed if there is a severe abnormality?

A

Intra-cytoplasmic sperm injection.

313
Q

How can infertility be managed if azoospermia is the cause?

A
  1. Surgical sperm recovery.

2. Donor insemination.

314
Q

Infertility: Give 3 risk factors for anovulation.

A
  1. Stress.
  2. Low weight.
  3. Extreme exercise.
  4. Kallmann’s + Turner’s syndrome.
315
Q

What is the rotterdam diagnostic criteria for PCOS.

A
  1. Anovulation/oligomenorrhoea.
  2. Polycystic ovaries seen on imaging.
  3. Increased androgens - clinically or biochemically.
316
Q

How can PCOS be treated?

A
  1. Encourage weight loss.
  2. COCP if not wanting to get pregnant.
  3. Symptomatic treatment of acne and hirsutism.
    For pregnancy:
  4. Clomifene/tamoxifen.
  5. Metformin.
  6. Ovarian drilling.
317
Q

How does Clomifene work in the treatment of PCOS?

A

Clomifene is an anti-oestrogen. It leads to increased production of LH/FSH and so there is more follicle stimulation. It can treat menstrual disturbance and has a good pregnancy rate.

318
Q

Infertility: give 3 causes of tubal disease.

A
  1. Infections.
  2. Endometriosis.
  3. Iatrogenic e.g. following surgery.
319
Q

Briefly describe the process of IVF.

A

Ovarian stimulation -> egg collection -> insemination -> fertilisation check -> embryo culture -> embryo transfer -> luteal support.

320
Q

Why is only 1 egg transferred in IVF?

A

To avoid multiple pregnancy.

321
Q

Give 4 risks associated with IVF.

A
  1. Multiple pregnancy.
  2. Miscarriage.
  3. Ectopic pregnancy.
  4. Foetal abnormality.
322
Q

Give 4 factors that can affect the likelihood of IVF being successful.

A
  1. Increasing age -> reduced egg quality.
  2. Successive cycles/longer duration infertility.
  3. Obesity.
  4. Environmental factors e.g. smoking, alcohol, caffeine.
323
Q

Give 3 examples of uterine abnormalities that can affect fertility.

A
  1. Endometrial polyps.
  2. Fibroids e.g. sub-mucous will significantly affect pregnancy rates.
  3. Adhesions.
324
Q

How can pregnancy affect anaemia?

A
  • 2-fold increase in iron requirements -> micro-cytic aneamia.
  • B12/folate deficiency -> macrocytic anaemia.
325
Q

By what percentage does cardiac output increase in pregnancy?

A

40%.

326
Q

If a lady with mechanical heart valves was pregnant what drug would you consider prescribing?

A

You would anti-coagulate the patient with LMWH as this does not cross the placenta.

327
Q

What inheritance pattern is associated with obstetric cholestasis?

A

Autosomal dominant.

328
Q

What symptoms does obstetric cholestasis often present with?

A

Itching! Typically on the palms and soles.

329
Q

What might you see on the blood results taken from a patient with obstetric cholestasis?

A

Raised AST, ALT and bile acid.

330
Q

What is there an increased risk of in women with obstetric choelstasis?

A

Still birth.

331
Q

What happens in women with gestational diabetes when extra glucose crosses the placenta?

A

Insulin, GF and GH’s are produced -> foetal growth is stimulated and fat and glycogen are deposited.

332
Q

Give 5 things a diabetic lady is at increased risk of if she is pregnant.

A
  1. Shoulder dystocia.
  2. Macrosomia.
  3. Amniotic excess - polyhydramnios.
  4. Stillbirth.
  5. Hypoglycaemia.
  6. Premature labour.
  7. Miscarriage.
  8. Foetal abnormalities.
333
Q

How can epilepsy in pregnancy be managed?

A
  • Pre-conception counselling is important.
  • Manage triggers and control seizures.
  • Medications are often very teratogenic e.g. sodium valporate.
  • Small risk of baby inheriting epilepsy.
334
Q

Define FGM.

A

Procedures involving damaging or removing external female genitalia for non-medical reasons.

335
Q

What problems can FGM cause?

A
  1. Problems with conception and labour.
  2. Increased risk of infections.
  3. PTSD.
  4. Chronic pain.
  5. Women are also at increased risk of needing a c-section, episiotomy and having PPH.
336
Q

Define primary amenorrhoea.

A

No menses by age 16 in the presence of secondary sexual characteristics or by age 14 with no secondary sexual characteristics.

337
Q

Define secondary amenorrhoea.

A

Cessation after the onset of menses. Can be due to weight loss, exercise, PCOS, pregnancy etc.

338
Q

Define oligomenorrhoea.

A

Menses >35 days apart.

339
Q

Define precocious puberty.

A

The onset of secondary sexual characteristics before 8 years old.

340
Q

What disease must you rule out in girls with delayed puberty and short stature?

A

Turner’s syndrome.

341
Q

What is endometriosis?

A

A chronic oestrogen dependent disease where there is growth of endometrial tissue outside of the endometrium.

342
Q

Why does endometriosis tend to get better after the menopause?

A

Endometriosis relies on oestrogen and so when oestrogen levels fall after the menopause the symptoms of endometriosis tend to improve.

343
Q

What hormone is responsible for ‘growing’ the endometrium and what hormone ‘shrinks’ the endometrium?

A

Oestrogen grows the endometrium and progesterone shrinks.

344
Q

Describe the epidemiology of endometriosis.

A

Endometriosis is more common in young, nulliparous women. Most girls present when their periods start.

345
Q

Describe the aetiology behind endometriosis.

A

The cause of endometriosis is thought to be due to retrograde menstruation and a genetic component. Lymphatic spread may also be responsible.

346
Q

What anatomical areas are most likely to be affected by endometriosis?

A

The pouch of douglas and the uterosacral ligaments.

347
Q

Give 5 risk factors for developing endometriosis.

A
  1. Early menarche.
  2. Late menopause.
  3. Delayed childbearing.
  4. Short cycles.
  5. Obstruction to vaginal flow.
  6. Genetic predisposition.
348
Q

Give 2 factors that are protective against endometriosis.

A
  1. Multiparity.

2. COCP.

349
Q

What is the gold standard investigation for diagnosing endometriosis?

A

Laparoscopy.

350
Q

What grading classification is used in endometriosis?

A

AFS classification.

351
Q

What investigations might you do in a woman who you suspect has endometriosis?

A
  1. Laparoscopy = gold standard.
  2. Digital exam.
  3. USS.
352
Q

Give 5 symptoms of endometriosis.

A
  1. Cyclic pain -> dysmenorrhoea and dyspareunia.
  2. Bleeding.
  3. Lump.
  4. Infertility.
  5. Dyschezia.

Remember: symptoms are often worse at certain times in a women’s cycle!

353
Q

Give 3 reasons why a woman with endometriosis might be infertile.

A
  1. Oocyte toxicity.
  2. Adhesions.
  3. Tubal and ovarian dysfunction.
354
Q

What non-specific protein marker might be raised in a woman with endometriosis?

A

CA125.

Non-specific, anything that irritates the peritoneum -> raised CA125.

355
Q

In what type of cancers is CA125 often raised?

A

Ovarian cancer (serous cancers).

356
Q

What tumour markers should be looked at in pre-menopausal women?

A

b-HCG, AFP and HDL.

357
Q

Briefly describe how the treatment for endometriosis works.

A

The pathology is oestrogen therefore remove the oestrogen or give an antagonist.

358
Q

What medications can be given to treat endometriosis?

A 
Abolish cyclicity:
1. OCP.
2. GnRH agonists.
Thin endometrium:
1. POP.
2. Mirena coil.
359
Q

Give 3 advantages of using the OCP to treat endometriosis.

A
  1. Cheap.
  2. Effective.
  3. Minimal side effects.
  4. Predictable and reliable.

Often 3 packs are taken back to back = ‘tri-phasing’ -> glandular atrophy.

360
Q

Describe how GnRH agonists work in treating endometriosis.

A

GnRH is normally released in a pulsatile way, GnRH agonists are given continuously in order to stop ovulation and triggers an ‘artificial menopause’ - this is reversible.

GnRH agonist -> huge release of FSH/LH -> down-regulation of FSH/LH -> no oestrogen release.

361
Q

Give 3 side effects of GnRH agonists being used to treat endometriosis.

A
  1. Osteoporosis.
  2. Hot flushes.
  3. Mood swings.
362
Q

Endometriosis treatment: how can the side effects of GnRH agonists be prevented?

A

A small dose of oestrogen should be prescribed - ‘add back’ e.g. livial (HRT).

363
Q

What drugs can cause endometrium glandular atrophy and so can be used in the treatment of endometriosis?

A

Progesterones e.g. POP, depot provera, mirena coil.

Coil is good because the progesterone is put directly in the uterus and so this reduces any systemic effects, the endometrium is thinned and also provides good contraception.

364
Q

How would you treat endometriosis in a woman who is wanting to get pregnant?

A

Surgery e.g. ablation and excision.

365
Q

Give 3 differentials for endometriosis.

A

Chronic pelvic pain:

  1. PID.
  2. Uterine fibroids.
  3. If older woman, adenomyosis.
  4. Ovarian cysts.
366
Q

What is adenomyosis?

A

The invasion of endometrial tissue into the myometrium.

367
Q

Give 3 risk factors for adenomyosis.

A
  1. Multi-parity.
  2. Uterine surgery.
  3. Previous caesarean section.

Adenomyosis is thought to occur after uterine damage.

368
Q

Describe the epidemiology of adenomyosis and compare it to that of endometriosis.

A

Adenomyosis: older, multiparous women.

Endometriosis: younger, nulliparous women.

369
Q

Give 3 symptoms of adenomyosis.

A
  1. Menorrhagia.
  2. Dysmenorrhoea.
  3. Dyspareunia.

Pain is typically cyclical.

370
Q

What investigations might you do to confirm a diagnosis after adenomyosis?

A
  1. Transvaginal USS.
  2. MRI.

Adenomyosis is difficult to diagnose with imaging, histology at hysterectomy is definitive.

371
Q

What is the treatment for adenomyosis?

A

Only curative treatment is hysterectomy.

Hormone therapy and analgesia can be used as conservative treatments.

372
Q

What are fibroids?

A

Benign smooth muscle tumours of the uterine myometrium.

373
Q

What hormone is thought to stimulate fibroid development?

A

Oestrogen.

374
Q

How are fibroids classified?

A

Fibroids are classified according tot heir position in the uterine wall, for example:

  • Intramural.
  • Sub-mucosal.
  • Sub-serosal.
375
Q

With regards to position in the uterine wall, what type of fibroids are most common?

A

Intramural - fibroids confined to the myometrium.

376
Q

Describe the location of sub-mucosal fibroids.

A

Fibroids growing into the uterine cavity.

377
Q

Describe the location of sub-serosal fibroids.

A

Fibroids growing outwards from the uterus.

378
Q

Give 4 risk factors for the development of fibroids.

A
  1. Obesity.
  2. Early menarche.
  3. Family history.
  4. Increasing age.
379
Q

Give 4 symptoms of fibroids.

A
  1. Pain.
  2. Infertility/sub-fertility.
  3. Menorrhagia.
  4. Pressure symptoms e.g. urinary frequency if pressing on bladder.
  5. Can cause iron deficiency anaemia -> lethargy and pallor.
380
Q

What investigations might you do to determine if a patient has fibroids?

A
  1. Pelvic USS.

2. Hysteroscopy.

381
Q

Describe the different treatment options for uterine fibroids.

A
  1. Conservative: watch and wait.
  2. Medical: hormone therapy e.g. POP. GnRH agonists.
  3. Surgical: hysteroscopic resection, myomectomy, hysterectomy.
382
Q

What is the gold standard treatment for uterine fibroids?

A

Hysterectomy.

If the patient is young and wants children then a myomectomy can be done.

383
Q

Give 3 differentials for uterine fibroids.

A
  1. Endometrial polyps.
  2. Cancer.
  3. Endometriosis/adenomyosis.
  4. Chronic PID.
384
Q

Describe a first degree vaginal tear.

A

First degree - tear within vaginal mucosa only.

385
Q

Describe a second degree vaginal tear.

A

Second degree - tear into sub-cutaneous tissue.

386
Q

Describe a third degree vaginal tear.

A

Third degree - laceration extends into external anal sphincter.

387
Q

Describe a fourth degree vaginal tear.

A

Fourth degree - laceration extends through external anal sphincter into rectal mucosa.

388
Q

Give 3 risk factor’s for vaginal tears.

A
  1. Primigravida.
  2. Macrosomia and shoulder dystocia.
  3. Forceps delivery.
389
Q

Define menopause.

A

The cessation of menstruation normally around 51 years old. Menopause is diagnosed retrospectively after 12 months of amenorrhoea or 12 months after the onset of symptoms if the patient has had a hysterectomy.

390
Q

Define peri-menopause.

A

The period leading up to the menopause. It is characterised by irregular periods and symptoms e.g. hot flushes, mood swings and urogenital atrophy.

391
Q

A depletion in what hormone is thought to trigger the symptoms of the menopause?

A

A reduction in oestrogen.

392
Q

Give 2 vasomotor symptoms of the menopause.

A
  1. Hot flushes.
  2. Night sweats.

This can impact on sleep, mood and QOL.

393
Q

Give 2 MSK symptoms of the menopause.

A
  1. Joint pain.

2. Muscle pain.

394
Q

Give 3 local affects of the menopause.

A

Vaginal atrophy ->

  1. Vaginal dryness.
  2. Dyspareunia.
  3. Recurrent UTI’s.
  4. PMB.
395
Q

Give 3 potential long term impacts of the menopause.

A
  1. Osteoporosis.
  2. CV disease.
  3. Dementia.
396
Q

Describe how the menopause can be managed in a symptomatic patient.

A
  1. Holistic approach, lifestyle advice, reduce modifiable RF’s.
  2. HRT, vaginal oestrogens.
  3. Non-hormonal options e.g. clonidine.
  4. Non-pharmaceutical e.g. CBT.
397
Q

Give 3 advantages of HRT being used to treat the menopause.

A
  1. Relief of symptoms.
  2. BMD protection.
  3. Prevents long term morbidity.
398
Q

Give 3 disadvantages of HRT being used to treat the menopause.

A
  1. Increased breast cancer risk.
  2. Increased VTE risk with oral HRT.
  3. Increased CV disease risk.
399
Q

What hormone should be given to women with a uterus who are prescribed HRT?

A

Progesterone.

This protects the endometrium from the stimulatory effects of unopposed oestrogen.

400
Q

When might transdermal HRT be indicated?

A
  1. Women with gastric problems e.g. crohn’s.
  2. Migraines/epilepsy sufferers.
  3. High risk VTE.
  4. Older women.
  5. Hypertensive patients.
  6. Patient choice.
401
Q

What is premature ovarian failure?

A

Primary ovarian insufficiency before the age of 40 with associated menopausal symptoms such as night sweats.

402
Q

What would hormone profile tests show in women with premature ovarian failure.

A

Low oestrogen and high FSH.

403
Q

What can cause premature ovarian failure?

A
  1. Idiopathic.
  2. Chromosomal abnormalities.
  3. Enzyme deficiencies.
  4. Autoimmune.
  5. Iatrogenic e.g. following surgery, chemotherapy, radiotherapy.
404
Q

What is the diagnostic criteria for premature ovarian failure?

A
  1. FSH >25IU/I – 2 samples 4 weeks apart.

2. 4 months of amenorrhoea.

405
Q

Describe the treatment for premature ovarian failure.

A

Oestrogen replacement e.g. HRT or COCP. Donor eggs for fertility.

406
Q

If a woman goes through the menopause <50 for how many years is she still fertile for?

A

2 years.

407
Q

If a woman goes through the menopause >50 for how many years is she still fertile for?

A

1 year.

408
Q

Define small for gestational age (SGA).

A

An infant born with an EBW <10th centile as plotted on a customised growth chart.

409
Q

Define large for gestational age (LGA).

A

An infant born with an EBW >90th centile as plotted on a customised growth chart.

410
Q

Define foetal macrosomia.

A

An infant with a birth weight >4000g.

411
Q

Define low birth weight.

A

An infant with a birth weight <2500g.

412
Q

Define foetal growth restriction.

A

An infant who does not reach its full potential.

413
Q

Give 5 potential causes of FGR.

A
  1. Poor weight gain during pregnancy.
  2. Poor nutrition and diet.
  3. Alcohol, drug use, smoking.
  4. Gestational diabetes.
  5. HTN and pre-eclampsia.
  6. Placental insufficiency.
414
Q

What investigation might you do if you are concerned about foetal growth restriction?

A

Clinical examination.

USS - HC, AC and FL.

415
Q

Define chronic pelvic pain.

A

Lower abdominal pain for >6m that does not occur exclusively with menstruation, intercourse or pregnancy.

416
Q

Define acute pelvic pain.

A

Sudden and unexpected pain for <6m.

417
Q

Give 3 pregnancy related causes of acute pelvic pain.

A
  1. Ectopic pregnancy.
  2. Miscarriage.
  3. Ovarian cyst rupture/haemorrhage/torsion.
418
Q

Give 3 gynaecological causes of acute pelvic pain.

A
  1. PID.
  2. Abscess.
  3. Ovarian cyst rupture/haemorrhage/torsion.
419
Q

Give 3 gastrointestinal causes of acute pelvic pain.

A
  1. Appendicitis.
  2. Constipation.
  3. Bowel obstruction.
420
Q

Give 3 genito-urinary causes of acute pelvic pain.

A
  1. UTI.
  2. Renal stones.
  3. Urinary retention.
421
Q

Give 2 MSK causes of acute pelvic pain.

A
  1. Disc prolapse.

2. Nerve entrapment.

422
Q

Give 5 gynaecological causes of chronic pelvic pain.

A
  1. Endometriosis/adenomyosis.
  2. Fibroids.
  3. Adhesions.
  4. PID.
  5. Ovarian cysts.
423
Q

Give 3 gastrointestinal causes of chronic pelvic pain.

A
  1. IBS.
  2. Constipation.
  3. Inflammatory bowel.
424
Q

Give a genito-urinary cause of chronic pelvic pain.

A

Interstitial cystitis.

425
Q

Give 2 MSK causes of chronic pelvic pain.

A
  1. Nerve entrapment.

2. Referred MSK pain.

426
Q

What investigations might you do on a patient who is presenting with pelvic pain?

A
  1. Pelvic USS -> fibroids, ovarian cysts, endometriosis.
  2. Laparoscopy -> endometriosis, adhesions.
  3. Hysteroscopy -> fibroids.
  4. MRI -> adhesions, adenomyosis, fibroids.
  5. STI screen.
427
Q

What can cause PID?

A

Infection e.g. gonorrhoea/chlamydia that ascends from the endocervix.

428
Q

Give 5 symptoms of PID.

A
  1. Lower abdominal pain.
  2. Dyspareunia.
  3. Abnormal vaginal bleeding e.g. post-coital, IMB, menorrhagia, abnormal discharge.
429
Q

Describe the treatment for PID.

A

IM ceftriaxone 500mg followed by PO doxycycline 100mg BD and PO metronidazole 400mg BD for 14 days.

430
Q

What layer of the tri-laminar disc forms the male and female genitalia?

A

Intermediate mesoderm.

431
Q

What does the müllerian duct form?

A
  1. Fallopian tubes.
  2. Uterus.
  3. Cervix.
  4. Proximal 1/3 of vagina.
432
Q

What does the cloaca divide into?

A
  1. Anorectal canal.

2. Urogenital sinus.

433
Q

From what artery are the ovarian arteries a branch of?

A

The abdominal aorta.

434
Q

Where do the L and R ovarian veins drain?

A

L ovarian vein -> L renal vein.

R ovarian vein -> IVC.

435
Q

Describe the hypothalamic gonadal axis.

A

Hypothalamus -> GnRH -> anterior pituitary -> FSH/LH -> Granulosa and Theca cells -> Androgens and Oestrogen.

436
Q

Amenorrhoea aetiology: give 3 hypothalamic causes.

A
  1. Reduced GnRH.
  2. Functional disorders e.g. eating disorders.
  3. Kallmann syndrome.
437
Q

Amenorrhoea aetiology: give 3 pituitary causes.

A
  1. Prolactinomas.
  2. Other pituitary tumours e.g. acromegaly and cushing’s.
  3. Sheehan’s syndrome (infarction of pituitary often due to PPH).
438
Q

Amenorrhoea aetiology: give 3 ovarian causes.

A
  1. PCOS.
  2. Turner’s (45X)
  3. Premature ovarian failure.
439
Q

Amenorrhoea aetiology: give 2 uterine causes.

A
  1. Imperforate hymen.

2. Müllerian agenesis.

440
Q

What is androgen insensitivity syndrome?

A

When a person is genetically male but phenotypically female. They have intra-abdominal gonads and their cells don’t respond to male hormones e.g. androgens.

441
Q

Amenorrhoea: what part of the hypothalamic gonadal axis would be affected if FSH/LH levels came back abnormal?

A

This could indicate a pituitary problem.

442
Q

Amenorrhoea: what part of the hypothalamic gonadal axis would be affected if GnRH levels came back abnormal?

A

This could indicate a hypothalamic problem.

443
Q

Give 2 signs of polyhydramnios.

A
  1. Increased abdominal size that is out of proportion for weight and gestation.
  2. AFI >20 on USS.
  3. Maternal dyspnoea and faint foetal heart sounds.
444
Q

Give 3 causes of polyhydramnios.

A
  1. Maternal diabetes.
  2. Foetal anomalies e.g. duodenal atresia.
  3. Multiple gestation.
445
Q

Give 3 potential consequences of polyhydramnios.

A
  1. Corp prolapse.
  2. PPH.
  3. Preterm labour.
  4. IUGR.
446
Q

Describe the management of obstetric cholestasis.

A
  1. Obstetrician lead care.
  2. Symptomatic relief for itch e.g. emollients, anti-histamines, cool showers.
  3. Ursodeoxycholic acid.
447
Q

What are the potential consequences of failing to treat pre-eclampsia?

A
  1. Eclampsia.
  2. HELLP syndrome.
  3. Renal/Liver failure.
  4. Premature labour.
  5. IUGR.
448
Q

Give 4 differentials for a breast lump.

A
  1. Breast carcinoma.
  2. Fibroadenoma.
  3. Breast abscess.
  4. Breast cyst.
449
Q

Give 4 investigations you might do in someone who you suspect has cervical cancer.

A
  1. Vaginal examination.
  2. Colposcopy.
  3. Biopsy.
  4. HPV Testing.
450
Q

Rhesus disease: name 3 events during pregnancy when sensitisation may occur.

A
  1. Miscarriage.
  2. Abortion.
  3. Amniocentesis.
  4. Placental abruption.
  5. During delivery.
451
Q

Name 3 factors that are protective against cervical cancer.

A
  1. Pregnancy.
  2. Breast feeding.
  3. COCP.
452
Q

Antenatal screening: What is the combined test?

A 
The combined test is done to check for congenital anomalies. It is made up of:
- PAPP-A
- bHCG
- Nuchal Translucency
- Mothers age
(Done at 11-14w).
453
Q

Antenatal screening: What is the quadruple test?

A

The quadruple test is useful for women presenting in the 2nd trimester. It looks for congenital anomalies. It is made up of:

  • bHCG
  • AFP
  • Inhibin A
  • Unconjugated oestradiol
454
Q

What chromosomal abnormality is found in Edward’s disease. Give 3 physical signs of this condition.

A

Edward’s = T18.

Signs: LBW, small head, small mouth/jaw, low set ears, cleft palate, exomphalos.

455
Q

What chromosomal abnormality is found in Patau’s disease. Give 3 physical signs of this condition.

A

Patau’s = T13.

Signs: cleft lip/palate, small eyes, microcephaly, ear malformations, rocker-bottom feet.

456
Q

A rhesus negative mum is having an amniocentesis. What must you give her prior to this procedure?

A

Anti-D!

There is a risk of sensitisation.

457
Q

Give 4 risks associated with amniocentesis.

A
  1. Miscarriage.
  2. Infection.
  3. Trauma.
  4. Bleeding.
  5. Sensitisation reaction.
  6. Pre-term labour.
458
Q

Give 3 indications for induction of labour.

A
  1. Post maturity.
  2. Pre-eclampsia.
  3. Diabetes.
  4. Growth restriction.
  5. Reduced foetal movements.
459
Q

What is Sheehan’s syndrome?

A

Pituitary infarction/necrosis following PPH. Can lead to reduced TSH, ACH, FSH/LH and so hypothyroidism and genital atrophy.

James' Phase 3A Medicine (5 decks)

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