Women's Health Flashcards

1
Q

Name 3 hormones that are important in pregnancy.

A

Main hormones:

hCG.
Progestins.
Oestrogens.
Other hormones:

hPL.
Prolactin.
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

Pre-eclampsia.
IUGR.
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

Pre-eclampsia.
IUGR.
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 induce labour.

A

Syntocinon.

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59
Q

Define: pelvic organ prolapse

A

Descent of the pelvic organs into the vagina

uterine prolapse = uterus

Vault prolapse = women who have a hysterectomy so vagina descends

Rectocele = rectum due to defect in peoterior vaginal wall

cystocele = bladder due to defect in anterior vaginal wall

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60
Q

What are the risk factors for prolapse?

A
  • multiple vaginal deliveries
  • instrumental, prolonged or traumatic delivery
  • Advanced age and postmenopause status
  • Obesity
  • Chronic respiratory disease causing coughing
  • Chronic constipation causing straining
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61
Q

Presentation: prolapse

A
  • A feeling of “something coming down” in the vagina
  • A dragging or heavy sensation in the pelvis
  • Urinary symptoms, such as incontinence, urgency, frequency, weak stream and retention
  • Bowel symptoms, such as constipation, incontinence and urgency
  • Sexual dysfunction, such as pain, altered sensation and reduced enjoyment
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62
Q

What are the grades of uterine prolapse?

A

Pelvic organ prolapse quantification (POP-Q)

Grade 0: Normal
Grade 1: The lowest part is more than 1cm above the introitus (external opening of vagina)
Grade 2: The lowest part is within 1cm of the introitus (above or below)
Grade 3: The lowest part is more than 1cm below the introitus, but not fully descended
Grade 4: Full descent with eversion of the vagina

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63
Q

Management: Prolapse

A
  1. conservative
    - pelvic floor exercises
    - weight loss
    - treat stress incontinence symptoms
    - vaginal oestrogen cream
  2. Vaginal pessary
    - inserted into vagina to give more support
  3. Surgery
    - repair anterior or posterior walls
    - sacro spinous fixation = stick top of vagina to ligament
    - sarocolpopexy = mesh in abdomen
    - Hysterectomy
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64
Q

What are the types of urinary incontinence?

A
  1. Stress = weakness of the pelvic floor and sphincter muscles
  2. Urge = overactivity of the detrusor muscle of the bladder
  3. Mixed
  4. Overflow = due to chronic urinary retention due to an obstruction to the outflow of urine
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65
Q

What are the risk factors for urinary incontinence?

A

Increased age
Postmenopausal status
Increase BMI
Previous pregnancies and vaginal deliveries
Pelvic organ prolapse
Pelvic floor surgery
Neurological conditions, such as multiple sclerosis
Cognitive impairment and dementia

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66
Q

Presentation: stress incontinence

A

involuntary leakage
- cough
- laughing
- lifting
- exercise
- movement
- intercourse
- walking/running downhill
(sphincter weakness)

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67
Q

Presentation: urgency incontinence

A

Overactive bladder
Urgency incontinence
Frequency
Nocturia
Nocturnal enuresis
‘Key in the door’
‘Handwash’
Intercourse

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68
Q
A
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69
Q

Investigations: urinary incontinence

A
  1. bladder diary
  2. urine dipstick testing
  3. post-void residual bladder volume
  4. urodynamic testing
    - measure detrusor muscle contraction
    - measure flow rate
    - measure pressure in bladder vs pressure in vagina/anus to calculate detrusor activity
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70
Q

What is the innervation of the detrusor muscle?

A

detrusor muscle
- smooth muscle, transitional epithelium

sacral parasympathetic (para pee) S2-4 = cause bladder wall to contract and sphincter to relax

neurotransmitter = acetylcholine

Receptors = muscarinic M2 + M3
Antagonists = atropine (oxybutynin, tolterodine)

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71
Q

Management: stress incontinence

A

Lifestyle
- Avoiding caffeine, diuretics and overfilling of the bladder
- smoking cessation
- Avoid excessive or restricted fluid intake
- Weight loss (if appropriate)

  • Supervised pelvic floor exercises for at least three months before considering surgery

Containment
- bladder bypass (catheters)
- leakage barrier (pads + pants)
- vaginal support (pessaries)
- skin care (barrier creams

  • Surgery
  • Duloxetine is an SNRI antidepressant used second line where surgery is less preferred
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72
Q

What are the mechanisms of mirabegnon?

A

Beta-3 adrenergic receptor agonist

Relaxes smooth muscle detrusor

Increases bladder capacity

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73
Q

Define: urinary tract calculi

A

Hard lumps of minerals that can from inside the bladder when its not completely empty of urine e.g. due to enlarged prostate gland

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74
Q

Presentation: urinary tract calculi

A
  • lower abdominal pain
  • pain or difficulty peeing
  • peeing more frequently
  • cloudy or dark coloured urine
  • blood
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75
Q

MAnagement: urinary tract calculi

A

Surgery
- cystolitholapaxy = cystoscope camera tube inserted and stones crushed

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76
Q

What are the most common types of uterine abnormalities?

A

Incomplete fusion of mullein or paramesonephric ducts
- lead to double vagina, cervix, uterus
- uterus with midline septum
- double single-horned uteruses

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77
Q

Investigations: uterine abnormalities

A
  • ultrasound
  • hysterosalpingography
  • MRI scan
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78
Q

Complications of uterine abnormalities?

A
  • dysmenorrhoea
  • haematometra
  • pregnancy + labour complications
  • fertility usually unaffected
  • congenital renal abnormalities
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79
Q

Management: uterine abnormalities

A
  • surgery = if affects viable pregnancy
  • uterine reconstruction
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80
Q

What types of vaginal abnormalities occur?

A
  1. Vaginal agenesis: absent uterus but ovaries present.
  2. Vaginal atresia:
    The lower portion of the vagina consists of fibrous tissue with a well-differentiated uterus.
  3. Müllerian aplasia:
    Nearly all of the vagina and most of the uterus are absent.
  4. Transverse vaginal septa:
    Can be present as single or multiple in the upper or lower segments and may be patent or perforated; can be the cause of haematometra or other fluid collections.
  5. Longitudinal vaginal septa
    anomalies:
    The urethra can open into the vaginal wall or the vagina can open into a persistent urogenital sinus.
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81
Q

Define: androgen insensitivity syndrome

A

Condition where the cells are unable to respond to androgen hormones due to a lack of androgen receptors

  • x- linked recessive
  • mutation in androgen receptor gene
  • extra androgens converted to oestrogen
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82
Q

Pathophysiology: androgen insensitivity syndrome

A
  • genetically male with XY
  • but female phenotype externally
  • extra androgens converted to oestrogen
  • patients have testes in abdomen or inguinal canal and absence of uterus, upper vagina, cervix, ovaries
  • due to testes producing anti-mullerian hormone
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83
Q

Presentation: androgen insensitivity syndrome

A
  • lack of pubic + facial hair
  • inguinal hernias at infancy containing testes
  • primary amenorrhoea
  • raised LH
  • normal or raised FSH
  • normal or raised testosterone levels (for a male)
  • raised oestrogen ( for a male)
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84
Q

Management: androgen insensitivity syndrome

A
  1. bilateral orchidectomy (removal of testes to avoid testicular tumour)
  2. oestrogen therapy
  3. vaginal dilators or vaginal surgery (to create an adequate vaginal length)
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85
Q

Define: menarche

A

First menstrual cycle
ages 11-15

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86
Q

What hormone changes occur in puberty?

A
  1. Hypothalamus releases Gonadotropin releasing hormone GnRH in a pulsatile manner
  2. stimulates release of LH and FSH from anterior pituitary gland
    (rise in FSH stimulates an increase in oestrogen synthesis + oogenesis + sperm production)
  3. FSH + LH act on gonads to stimulate synthesis of sex steroid hormones (oestrogen/progesterone and testosterone)
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87
Q

What are the physical changes in females in puberty?

A
  1. Thelarche = breast development aged 9-10
  2. Pubarche = growth of public hair
  3. Menarche = first period
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88
Q

What are the physical changes in males in puberty?

A
  1. genital changes = increased testicular size
    - Increased LH stimulates testosterone synthesis by Leydig cells
    - Increased FSH stimulates sperm production by Sertoli cells
    - scrotal skin becomes thinner and darker
    - ejaculation then occurs
    - penis then grows in length then width
  2. pubarche = growth of pubic hair
  3. Growth spurt
    -rise in GH and IGF-1
    - larynx and vocal cords enlarge
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89
Q

What are the stages of menopause?

A

Premature menopause = before age of 40 yrs

Perimenopause = time around the menopause and 12 months after last period

Menopause = point at which menstruation stops

Postmenopause = period from 12 months after the final menstrual period

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90
Q

What happens to hormones during menopause?

A

Lack of ovarian follicular function
- Oestrogen low
- progesterone low
- LH + FSH high (lack of feedback from oestrogen)

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91
Q

What is the process that starts menopause?

A
  1. reduced development of ovarian follicles
  2. reduced production of oestrogen
  3. Absence of negative feedback from oestrogen
  4. LH and FSH increase
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92
Q

What are some perimenopausal symptoms?

A
  • Hot flushes
  • Emotional lability or low mood
  • Premenstrual syndrome
  • Irregular periods
  • Joint pains
  • Heavier or lighter periods
  • Vaginal dryness and atrophy
  • Reduced libido
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93
Q

What does a lack of oestrogen increase the risk of?

A

Cardiovascular disease and stroke
Osteoporosis
Pelvic organ prolapse
Urinary incontinence

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94
Q

What is contraception advice for menopausal women?

A

Still need to use contraception until:
- 2 yrs after last period in women <50 yrs
- 1 yrs after last period in women >50 yrs

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95
Q

Management: perimenopausal symptoms

A
  • No treatment
  • Hormone replacement therapy (HRT)
  • Tibolone = synthetic steroid hormone that acts as continuous combined HRT (only after 12 months of amenorrhoea)
  • Clonidine = agonists of alpha-adrenergic and imidazoline receptors
  • Cognitive behavioural therapy (CBT)
  • SSRI antidepressants = fluoxetine or citalopram
  • Testosterone can be used to treat reduced libido (usually as a gel or cream)
  • Vaginal oestrogen cream or tablets = help with vaginal dryness and atrophy (can be used alongside systemic HRT)
  • Vaginal moisturisers = Sylk, Replens and YES
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96
Q

Define: adenomyosis

A

Endometrial tissue inside the myometrium (muscle layer of uterus)

  • usually later in life after several pregnancies
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97
Q

Presentation: adenomyosis

A
  1. Painful periods (dysmenorrhoea)
  2. Heavy periods (menorrhagia)
  3. Pain during intercourse (dyspareunia)
  • infertility or pregnancy complications
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98
Q

Investigations: adenomyosis

A
  1. transvaginal USS
  2. transabdominal USS
  3. MRI

gold standard diagnosis = Hysterectomy with histology

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99
Q

Management: adenomyosis

A

Contraception wanted/acceptable
1. Mirena coil
2. combined oral contraceptive pill
3. cyclical oral progesterones

No contraception
1. tranexamic acid = when no associated pain, reduced bleeding
2. Mefenamic acid = reduced pain + bleeding

  • GnHR analogues induce menopause like state
  • endometrial ablation
  • uterine artery embolisation
  • hysterectomy
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100
Q

What is the effect of adenomyosis on pregnancy?

A

Infertility
Miscarriage
Preterm birth
Small for gestational age
Preterm premature rupture of membranes
Malpresentation
Need for caesarean section
Postpartum haemorrhage

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101
Q

Define: Asherman’s syndrome

A

Adhesions form within the uterus following damage to the uterus

  • Occurs after pregnancy related dilatation + curettage procedure (remove tissue left behind)
  • uterine surgery
  • pelvic infections
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102
Q

Presentation: Asherman’s syndrome

A
  • Secondary amenorrhoea (absent periods)
  • Significantly lighter periods
  • Dysmenorrhoea (painful periods)

May present with infertility

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103
Q

Investigations: Asherman’s syndrome

A
  • Gold standard = Hysteroscopy (can involved dissection + treatment)
  • Hysterosalpingography = contrast injected into uterus + imaged with x-rays
  • Sonohysterography = uterus filled with fluid + pelvic USS performed
  • MRI scan
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104
Q

Management: Asherman’s syndrome

A

Hysteroscopy
- dissect adhesions

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105
Q

Define: Lichen Sclerosis

A

Chronic inflammatory skin condition
- commonly affects labia, perineum, and perianal skin in women
- men = foreskin and glans of penis

  • autoimmune conditions
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106
Q

Presentation: lichen sclerosis

A
  • patches of shiny, porcelain white skin
  • itching
  • soreness + pain
  • skin tightness
  • painful sex
  • erosions
  • fissures
  • papules or plaques
  • slightly raised
    Koebner phenomenon = symptoms made worse by friction to skin
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107
Q

Management: lichen sclerosis

A
  1. potent topical steroids = clobetasol propionate (long term use)
  2. Emollients
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108
Q

What are the complications of lichen sclerosis?

A

Squamous cell carcinoma of the vulva

  • pain + discomfort
  • sexual dysfunction
  • bleeding
  • narrowing of the vagina or urethral openings
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109
Q

Define: Atrophic vaginitis

A

Dryness and atrophy of the vaginal mucosa related to a lack of oestrogen

  • occurs in women entering menopause
  • oestrogen causes epithelial to be thicker, more elastic and produce secretions
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110
Q

Presentation: Atrophic vaginitis

A

Itching
Dryness
Dyspareunia (discomfort or pain during sex)
Bleeding due to localised inflammation

Signs
- pale mucosa
- thin skin
- reduced skin folds
- erythema + inflammation
- dryness
- sparse pubic hair

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111
Q

MAnagement: Atrophic vaginitis

A
  1. vaginal lubricants = Sylk, Replens, YES
  2. Topical oestrogen
    - estriol cream, pessaries, tablets, ring

(SE = breast cancer, angina, venous thromboembolism)

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112
Q

Define: Vulval cancer

A

90 % = squamous cell carcinoma

less likely = malignant melanomas

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113
Q

What are the risk factors for vulval cancer?

A

Advanced age (particularly over 75 years)
Immunosuppression
Human papillomavirus (HPV) infection
Lichen sclerosus

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114
Q

Define: vulval intraepithelial neoplasia

A

Premalignant condition affecting the squamous epithelium of the skin
- watch + wait
- wide local excision
- imiquimod cream
- laser ablation

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115
Q

Presentation: vulval cream

A

Vulval lump
Ulceration
Bleeding
Pain
Itching
Lymphadenopathy in the groin
Labia majora = irregular mass, fungating lesion

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116
Q

Management: vulval cancer

A
  1. 2 week wait urgency cancer referral
  2. Biopsy of lesion
  3. Sentinel node biopsy = demonstrate lymph node spread FIGO
    4.wide local excision to remove cancer
  4. groin lymph node dissection
  5. chemo + radiotherapy
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117
Q

What is the cell type and cause of cervical cancer?

A

80% squamous cell carcinoma
Then adenocarcinoma

Cause = human papilloma virus (STI)
- p53 and pRb are tumour suppressor genes
- HPV produces E6 and E7 that inhibit these tumour suppressor genes

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118
Q

What are the risk factors for cervical cancer?

A

Increased risk of HPV
- early sexual activity
- multiple sexual partners
- not using condoms

Non-engagement with cervical screening

  • smoking
  • HIV
  • COCO pill
  • increased number of full term pregnancies
  • family history
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119
Q

Presentation: cervical cancer

A
  • Abnormal vaginal bleeding (intermenstrual, postcoital or post-menopausal bleeding)
  • Vaginal discharge
  • Pelvic pain
  • Dyspareunia (pain or discomfort with sex)
  • ulceration
  • bleeding
  • visible tumour
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120
Q

Investigations: cervical cancer

A

Smear test:
- cervical smear test every 3 years aged 25-49 then every 5 yrs
- test involves collecting cells from the cervix using a small brush

Colposcopy
- inserting a speculum to magnify cervix
- stains (acetic acid + iodine solution) used to differentiate abnormal areas

Large loop excision of the transformation zone
- loop of wire with electrical current to remove abnormal epithelial tissue on the cervix

Cone biopsy
- cone shaped piece of cervix removed using a scalpel
- sent for histology

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121
Q

What is the staging for obs+gynae cancers?

A

The International Federation of Gynaecology and Obstetrics (FIGO)

Stage 1: Confined to the cervix
Stage 2: Invades the uterus or upper 2/3 of the vagina
Stage 3: Invades the pelvic wall or lower 1/3 of the vagina
Stage 4: Invades the bladder, rectum or beyond the pelvis

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122
Q

Management: cervical cancer

A

Cervical intraepithelial neoplasia and early-stage 1A: LLETZ or cone biopsy

Stage 1B – 2A: Radical hysterectomy and removal of local lymph nodes with chemotherapy and radiotherapy

Stage 2B – 4A: Chemotherapy and radiotherapy

Stage 4B: Management may involve a combination of surgery, radiotherapy, chemotherapy and palliative care

Pelvic exenteration = advancesd, removes most of pelvic organs

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123
Q

What strains does the HPV vaccine protect against and what would these strains cause otherwise?

A

Given to girls and boys before becoming sexually active

Gardasil vaccine

strains 6 &11 =genital warts
strains 16 & 18 = cervical cancer

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124
Q

What is human papilloma virus?

A

DNA virus
- can infect all types of squamous epithelium
- high risk types = 16 + 18
- low risk types = 6 +11 > cause genital warts

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125
Q

Presentation: HPV

A

presence of new lumps/growths in the anogenital area
- cauliflower like growths
- flat, plaques
- pigmented
-

generally IP between 3-8 weeks

local irritation
bleeding
discomfort/itching

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126
Q

Management: HPV

A

Physical ablation
- excision
- cryotherapy
- electrosurgery
- laser treatment

Topical applications
- Podophyllotoxin (Warticon® and Condyline®)
- Imiquimod 5% cream
- Catephen® 10% ointment
- TCA 80-90% (specialist clinic setting only)

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127
Q

What is the most likely type of endometrial cancer?

A

Adenocarcinoma

oestrogen dependent cancer = oestrogen stimulates the growth of endometrial cancer cells

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128
Q

Define: endometrial hyperplasia

A

precancerous condition involving thickening of the endometrium
(less than 5% become endometrial cancer)

worrying types
- hyperplasia without atypia
- atypical hyperplasia

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129
Q

Treatment: endometrial hyperplasia

A

Using progesterones
- intrauterine system e.g. mirena coil
- continuous oral progesterones

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130
Q

What are the risk factors for endometrial cancer?

A

Unoppoed oestrogen = oestrogen without progesterone (as stimulates the endometrial cells)

  • Increased age
  • Earlier onset of menstruation
  • Late menopause
  • Oestrogen only hormone replacement therapy
  • No or fewer pregnancies
  • Obesity = adipose tissue is a source of oestrogen
  • Polycystic ovarian syndrome = increased exposure to unopposed oestrogen due to lack of ovulation (less progesterone released)
  • Tamoxifen = oestrogenic effect in endometrium
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131
Q

What are protective factors against endometrial cancer?

A

(most increase progesterone)

Combined contraceptive pill
Mirena coil
Increased pregnancies
Cigarette smoking = anti-oestrogenic, oestrogen metabolised differently, smokers thinner

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132
Q

Presentation: endometrial cancer

A
  1. postmenopausal bleeding

Postcoital bleeding
Intermenstrual bleeding
Unusually heavy menstrual bleeding
Abnormal vaginal discharge
Haematuria
Anaemia
Raised platelet count

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133
Q

What is the referral criteria for endometrial cancer?

A

2-week-wait urgent cancer referral:

  1. Postmenopausal bleeding (more than 12 months after the last menstrual period)

NICE also recommends referral for a transvaginal ultrasound in women over 55 years with:

  1. Unexplained vaginal discharge
  2. Visible haematuria plus raised platelets, anaemia or elevated glucose levels
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134
Q

Investigations: endometrial cancer

A
  • transvaginal USS for endometrial thickness (normal <4mm post menopause)
  • Pipelle biopsy = highly sensitive, sample from uterus
  • Hysteroscopy with endometrial biopsy
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135
Q

Management: endometrial cancer

A

Stage 1 + 2:
Total abdominal hysterectomy with bilateral salpingo-oophorectomy (uterus, cervix, adnexa)

Other:
- radical hysterectomy
- radiotherapy
- chemotherapy
- progesterones hormone treatment

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136
Q

What are the types of ovarian cancer?

A
  1. epithelial cell tumours MC
  2. Dermoid cysts/ germ cell tumours
    - benign ovarian tumours
    - associated with ovarian torsion
    - germ cells may cause raised a-FP and hCG
  3. Sex cord stromal tumours
    - benign or malignant
  4. Metastasis
    - Krukenberg tumour = metastasis form GI tract cancer
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137
Q

What are the risk factors for ovarian cancer?

A

Age (peaks age 60)
BRCA1 and BRCA2 genes (consider the family history)
Increased number of ovulations
Obesity
Smoking
Recurrent use of clomifene

( factors that increase number of ovulations, increase risk of ovarian cancer e.g. late menopause, early onset periods, no pregnancies)

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138
Q

Presentation: ovarian cancer

A

Can present with non-specific symptoms

Abdominal bloating
Early satiety (feeling full after eating)
Loss of appetite
Pelvic pain
Urinary symptoms (frequency / urgency)
Weight loss
Abdominal or pelvic mass
Ascites

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139
Q

What is the referral criteria for ovarian cancer?

A

2 week wait
- ascites
- pelvic mass
- abdominal mass

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140
Q

Investigations: ovarian cancer

A
  1. CA125 blood test (>35 is significant)
  2. pelvic USS
  3. CT scan
  4. histology using CT guided biopsy
  5. Paracentesis for ascitic fluid

women under 40 with complex ovarian masss check
- alpha fetoprotein (a-FP)
- human chorionic gonadotropin (HCG)

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141
Q

What are the causes of raised CA125?

A

Endometriosis
Fibroids
Adenomyosis
Pelvic infection
Liver disease
Pregnancy

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142
Q

Management: ovarian cancer

A

specialist gynaecologist oncology MDT
- surgery
- chemotherapy

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143
Q

Define: dysfunctional uterine bleeding

A

Abnormal uterine bleeding in the absence of organic disease
- usually presents with menorrhagia (heavy) without any cause

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144
Q

What are the causes of menorrhagia?

A
  • Dysfunctional uterine bleeding (no identifiable cause)
  • Extremes of reproductive age
  • Fibroids
  • Endometriosis and adenomyosis
  • Pelvic inflammatory disease (infection)
  • Contraceptives, particularly the copper coil
  • Anticoagulant medications
  • Bleeding disorders (e.g. Von Willebrand disease)
  • Endocrine disorders (diabetes and hypothyroidism)
  • Connective tissue disorders
  • Endometrial hyperplasia or cancer
  • Polycystic ovarian syndrome
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145
Q

What are the structural and non-structural differential diagnoses of menorrhagia?

A

Structural = PALM
- Polyp adenomyosis
- Leiomyoma (fibroids)
- Malignancy and hyperplasia

Non-structural = COEIN
- Coagulopathy Ovulatory dysfunction
- Endometrial
- Iatrogenic
- Not yet classified

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146
Q

What are the key questions in menorrhagia history?

A

Age at menarche
Cycle length, days menstruating and variation
Intermenstrual bleeding and post coital bleeding
Contraceptive history
Sexual history
Possibility of pregnancy
Plans for future pregnancies
Cervical screening history
Migraines with or without aura (for the pill)
Past medical history and past drug history
Smoking and alcohol history
Family history

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147
Q

What are the red flags for bleeding?

A
  • post menopausal bleeding
  • bleeding during pregnancy
  • pelvic mass
  • haemodynamically unstable
  • USS findings of thickness of endometrium (>12mm pre menopausal and >5mm peri-menopausal)
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148
Q

Investigations: Menorrhagia

A
  1. pelvic examination with a speculum and bimanual
  2. FBC = iron deficiency anaemia
  3. outpatient hysteroscopy = submucosal fibroids, endometrial pathology, persistent intermenstrual bleeding
  4. Pelvic + transvaginal USS = fibroids, adenomyosis

Swabs
coagulation screen
ferritin
thyroids function tests

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149
Q

Management: menorrhagia

A

Exclude pathology

No contraception
- tranexamic acid = reduce bleeding
- mefenamic acid = reduce bleeding + pain

Contraception
1. mirena coil
2. Combined oral contraceptive pill
3. Cyclical oral progesterones

Final: Endometrial ablation + hysterectomy

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150
Q

What are the terms used for variations in menstrual bleeding?

A

Irregular = metrorrhagia
absent = amenorrhea
frequent = polymenorrhea
infrequent = oligomenorrhoea
heavy = menorrhagia
Painful periods = dysmenorrhoea

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151
Q

Define: endometriosis

A

ectopic endometrial tissue outside the uterus

a lump of endometrial tissue outside uterus = endometrioma

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152
Q

What is the cause of endometriosis?

A

No clear cause just a few theories
1. Retrograde menstruation = during menstruation endometrial lining flows backwards through the Fallopian tubes and seeds itself around the pelvis

  1. embryonic cells meant to become endometrial tissue remain outside uterus
  2. spread of cells through lymphatic system
  3. metaplasia = cells outside uterus change
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153
Q

What is the pathophysiology of the symptoms of endometriosis?

A

Main symptom = pelvic pain

  1. endometrial tissue outside uterus still responds to hormones and bleeds in menstruation
  2. causing inflammation + irritation of tissue around the bleeding
  3. deposits in bladder or bowel can lead to blood in urine or stools
  4. can lead to adhesions = due to scar tissue from inflammation
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154
Q

Presentation: endometriosis

A
  • Cyclical abdominal or pelvic pain (pain only during menstruating)
  • Deep dyspareunia (pain on deep sexual intercourse)
  • Dysmenorrhoea (painful periods)
  • Infertility
  • Cyclical bleeding from other sites, such as haematuria
  • associated with IBS (follow ROME criteria to ensure endometriosis instead of IBS)

examination :
- Endometrial tissue visible in the vagina on speculum examination, particularly in the posterior fornix
- A fixed cervix on bimanual examination
- Tenderness in the vagina, cervix and adnexa

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155
Q

Investigations: endometriosis

A
  1. Examination
  2. pelvic USS
  3. Laparoscopic surgery (gold standard) = can remove deposits
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156
Q

Management: Endometriosis

A
  1. analgesia
  2. hormonal management = combined pill, POP pill, implant, coil, injections
    - Zolendax (triggers menopause)
    (can stop ovulation + reduce endometrial thickening)
    (if pain goes away with these then can diagnose with endometriosis)
  3. surgical
    - laparoscopic surgery (50% see nothing)
    - hysterectomy
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157
Q

Define: fibroids

A

Benign tumours of the smooth muscle of the uterus

also known as Uterine leiomyomas

Oestrogen sensitive

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158
Q

What are the types of fibroids?

A
  • intramural = within the myometrium
  • subserosal = just below the outer layer of the uterus, fill abdominal cavity
  • submucosal = just below the lining of the uterus (endometrium)
  • pedunculated = means on a stalk
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159
Q

Presentation: fibroids

A

Often asymptomatic

  • Heavy menstrual bleeding (menorrhagia) MC
  • Prolonged menstruation, >7 days
  • Abdominal pain = worse during menstruation
  • Bloating or feeling full in the abdomen
  • Urinary or bowel symptoms due to pelvic pressure or fullness
  • Deep dyspareunia (pain during intercourse)
  • Reduced fertility
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160
Q

Investigations: fibroids

A
  1. Hysteroscopy = for submucosal fibroids with menorrhagia
  2. pelvic USS = larger fibroids
  3. MRI scan = before surgery
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161
Q

Management: Fibroids

A

Fibroids <3cm
1. Mirena coil
2. symptomatic management with NSAIDs + tranexamic acid
3. combined pill
4. Cyclical oral progesterones
5. Surgical = endometrial ablation, resection, hysterectomy

Fibroids >3cm
1. refer to gynaecologist
2. Symptomatic management = NSAIDs and tranexamic acid
3. Mirena coil – depending on the size and shape of the fibroids and uterus
4. Combined oral contraceptive
5. Cyclical oral progestogens
6. Surgical
- uterine artery embolisation
- Myomectomy
- Hysterectomy

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162
Q

Define: Ovarian cyst

A

A fluid filled sac

  • premenopausal = usually benign, fluctuate with hormones
  • post menopausal = concern for malignancy
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163
Q

What does a diagnosis of PCOS require?

A

Two of:
- Anovulation
- Hyperandrogenism
- Polycystic ovaries on USS

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164
Q

Presentation: ovarian cysts

A

Most are asymptomatic

Pelvic pain
Bloating
Fullness in the abdomen
A palpable pelvic mass (particularly with very large cysts such as mucinous cystadenomas)

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165
Q

What are the types of functional cysts?

A
  1. Follicular cysts = represent the follicle, persist after egg is released, usually disappear after a few menstrual cycles
  2. Corpus luteum cysts
    - occur when corpus luteum fails to break down + instead fills with fluid
    - often seen in early pregnancy
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166
Q

Investigations: ovarian cysts

A

premenopausal with cyst < 5cm on USS no further investigations needed

  1. USS
  2. Bloods = CA125, LDH, a-FP, HCG
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167
Q

Management: ovarian cysts

A
  1. rule out ovarian cancer
  2. dermoid cysts = refer to gynaecologist
  3. simple ovarian cysts in premenopausal women
    <5cm = no follow up
    5-7 cm = routine referral to gynaecologist + yearly USS
    >7cm = MRI scan, surgical evaluation
  4. Postmenopausal women
    - CA125 bloods, refer to gynaecologist (ovaries not functioning so shouldn’t develop cysts)
    - Then CT scan
  5. surgery
    - ovarian cystectomy
    - oophorectomy
    (never drain as will refill)
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168
Q

What is a cyst accident?

A
  • includes rupture, haemorrhage and torsion
  • cyst rupture + haemorrhage occurs with functional cysts and are generally self-limiting
  • laparoscopy = required if diagnosis uncertain or patient haemodynamically unstable
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169
Q

Define: Meig’s syndrome

A

Triad of :
1. Ovarian fibroma (a type of benign ovarian tumour)
2. Pleural effusion
3. Ascites

Usually in older women
Removal of tumour = complete resolution

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170
Q

Define: ovarian torsion

A

Ovary twists in reaction to the surrounding connective tissue, Fallopian tube and blood supply

  • usually due to an ovarian mass > 5cm
  • more likely with benign tumours and in pregnancy
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171
Q

Presentation: ovarian torsion

A

Sudden onset severe unilateral pelvic pain
- constant
- gets progressively worse
- nausea and vomiting
- often non-specific (can assume its appendicitis)

examination
- localised tenderness
- palpable mass

Seen in women of reproductive age and can occur in pregnancy

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172
Q

Investigations: ovarian torsion

A
  1. pelvic USS = whirlpool sign, free fluid in pelvis, and oedema of the ovary
  2. Laparoscopic surgery = definitive diagnosis
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173
Q

Management: ovarian torsion

A
  1. emergency admission
  2. laparoscopic surgery
    - un-twist ovary and fix it in place (detorsion)
    - remove affected ovary (oophorectomy)
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174
Q

Define: Pelvic inflammatory disease

A

Inflammation and infection of the organs of the pelvis caused by infection spreading up through the cervix

Endometritis = inflammation of the endometrium
Salpingitis = fallopian tubes
Oophoritis = ovaries
Parametritis = parametrium, (connective tissue around the uterus)
Peritonitis = peritoneal membrane

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175
Q

What are the causes of pelvic inflammatory disease?

A

Usually STI
- Chlamydia trachomatis MC
- Neisseria gonorrhoeae (tends to produce more severe PID)
- Mycoplasma genitalium

other:
- gardnerella vaginalis
- haemophilus influenzae
- E.coli

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176
Q

What are the risk factors for inflammatory pelvic disease?

A

Not using barrier contraception
Multiple sexual partners
Younger age
Existing sexually transmitted infections
Previous pelvic inflammatory disease
Intrauterine device (e.g. copper coil)

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177
Q

Presentation: pelvic inflammatory disease

A

Pelvic or lower abdominal pain
Abnormal vaginal discharge
Abnormal bleeding (intermenstrual or postcoital)
Pain during sex (dyspareunia)
Fever
Dysuria
(usually young person)

Examination findings may reveal:

Pelvic tenderness
Cervical motion tenderness (cervical excitation)
Inflamed cervix (cervicitis)
Purulent discharge

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178
Q

Investigations: pelvic inflammatory disease

A
  1. check for STIs
    - NAAT swabs
    - HIV test
    - syphilis test
  2. high vaginal swab = send to lab
  3. pregnancy test = exclude ectopic pregnancy
  4. inflammatory markers = ESR + CRP raised
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179
Q

Management: pelvic inflammatory disease

A
  1. antibiotics
    - 14 days course
    - single IM ceftriaxone
    - plus PO doxycycline + metronidazole

avoid sexual intercourse until patient and partner completed treatment

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180
Q

Define: Fitz-Hugh-Curtis syndrome

A

Complication of pelvic inflammatory disease

  • inflammation and infection of the liver capsule
  • leads to adhesions between liver and peritoneum
  • bacteria may spread from pelvis via cavity, lymphatic system or blood

Presentation
- RUQ pain referred to right shoulder tip

Laparoscopy
Adhesiolysis = to treat adhesions

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181
Q

Define: Polycystic ovarian syndrome

A

common condition causing metabolic and reproductive problems in women

  • multiple ovarian cysts
  • infertility
  • oligomenorrhoea (irregular infrequent)
  • hyperandrogegism
  • insulin resistance
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182
Q

What is the Rotterdam criteria?

A

2 are required to diagnose PCOS:

  1. oligoovulation or an ovulation (irregular or absent periods)
  2. hyperandrogegism (hirsutism and acne)
  3. Polycystic ovaries on USS
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183
Q

Presentation: PCOS

A

Oligomenorrhoea or amenorrhoea
Infertility
Obesity (in about 70% of patients with PCOS)
Hirsutism
Acne
Hair loss in a male pattern

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184
Q

What are some complications of PCOS?

A
  • Insulin resistance and diabetes = high levels of insulin increase androgens released + halt development of follicles in ovaries
  • Acanthosis nigricans = thickened, rough skin
  • Cardiovascular disease
  • Hypercholesterolaemia
  • Endometrial hyperplasia and cancer
  • Obstructive sleep apnoea
  • Depression and anxiety
  • Sexual problems
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185
Q

Investigations: PCOS

A
  1. Blood tests:
    - Raised Testosterone
    - Sex hormone-binding globulin
    - Raised LH
    - FSH = high LH to FSH ratio
    - Prolactin (may be mildly elevated in PCOS)
    - Thyroid-stimulating hormone
    - raised insulin
    - normal/raised oestrogen

2.- Pelvic USS
- transvaginal USS - gold standard

  1. Oral glucose tolerance test
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186
Q

What diagnostic criteria is used for PCOS in USS?

A

String of pearls appearance

Either:
- 12 or more developing follicles in one ovary
- ovarian volume > 10cm3

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187
Q

Management: PCOS

A
  1. reduce risks associated with obesity, type 2 diabetes, hypercholersterolaemia and cardiovascular disease
  2. manage risk of endometrial cancer
    - mirena coil
    - induce a withdrawal bleed with COCP or cyclical progesterones
  3. manage infertility
  4. manage hirsutism
    - Co-cyprindiol (Dianette) COCP
  5. Manage acne
    - COCP
    - topical adapalene (retinoid)
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188
Q

What is the perinatal mental health period?

A
  • preconception
  • during pregnancy
  • mental health for the first 12 months after birth
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189
Q

What are the different stage of poor mental health in postpartum?

A

Baby blues = majority of women in 1st week (10 days)

Postnatal depression = 1in10, peak around 3 months after birth

Puerperal psychosis = 1in1000, few weeks after birth

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190
Q

What is the puerperium?

A

it is defined as the 6 week period immediately after the birth
- mother’s body physiological returns to pre-pregnancy state

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191
Q

What family history do you ask for in a postnatal mental health risk assessment?

A
  • schizophrenia
  • bipolar
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192
Q

What are the red flags signs for perinatal mental health?

A

Suicidal ideation
Feelings of incompetence as a parent
Estrangement from child
Hallucinations

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193
Q

Presentation: Baby blues

A

Mood swings
Low mood
Anxiety
Irritability
Tearfulness

Baby blues may be the result of a combination of:

Significant hormonal changes
Recovery from birth
Fatigue and sleep deprivation
The responsibility of caring for the neonate
Establishing feeding
All the other changes and events around this time

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194
Q

Presentation: Postnatal depression

A

Triad:
1. low mood
2. anhedonia (lack of pleasure in activities)
3. low energy

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195
Q

What screening tool is used for postnatal depression?

A

Edinburgh scale
Patient health Questionnaire-9

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196
Q

Management: postnatal depression

A

Mild cases = additional support, self-help, GP

Moderate = antidepressants SSRI + CBT

Severe = specialist psychiatry services, mother + baby unit

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197
Q

What are the features of pathological anxiety in perinatal period?

A

chronic excessive worry (not situational)
Hyperarousal

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198
Q

Investigations: Perinatal anxiety

A

Screening:
Generalised Anxiety Disorder-2

Diagnosis:
GAD-7

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199
Q

What are common anxiety disorders during perinatal period?

A

Generalised anxiety

PTSD - flashbacks

Obsessive compulsive disorder - Intrusive thoughts, ideas or images which a woman finds distressing

Tocophobia - Morbid dread and fear of childbirth, Primary/secondary

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200
Q

Management: Anxiety

A

MDT
Behavioural
Medication - Anti-depressants
Benzodiazepines
- Associated with cleft palate, neonatal withdrawal syndrome & floppy baby syndrome
- Short term management of symptoms
- Lowest dose possible for shortest time possible
- Avoid in third trimester

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201
Q

Presentation: Puerperal psychosis

A

Insomnia, tearful and agitated at first
Delusions
Hallucinations
Depression
Mania
Confusion
Thought disorder

most present within in first 3 months

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202
Q

Management: Puerperal psychosis

A

emergency

  1. Admission to the mother and baby unit (need bonding to continue, baby is protective factor)
  2. Cognitive behavioural therapy
  3. Medications (antidepressants, antipsychotics (not teratogenic) or mood stabilisers)
  4. Electroconvulsive therapy (ECT)
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203
Q

What are the associated risks of antipsychotics in pregnancy?

A

Used: olanzapine = increased risk of weight gain, gestational diabetes

NOT USED
Lithium = cardiac abnormalities
Sodium valproate = neural tube defects

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204
Q

Define: ectopic pregnancy

A

A pregnancy that is implanted outside the uterus

  • MC in the Fallopian tube
  • Also in ovary, cervix, abdomen
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205
Q

What are the risk factors for an ectopic pregnancy?

A

Previous ectopic pregnancy
Previous pelvic inflammatory disease
Previous surgery to the fallopian tubes
Intrauterine devices (coils)
Older age
Smoking

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206
Q

Presentation: Ectopic Pregnancy

A

6- 8 weeks pregnant

  • Missed period
  • Constant lower abdominal pain in the right or left iliac fossa
  • Vaginal bleeding
  • Lower abdominal or pelvic tenderness
  • Cervical motion tenderness (pain when moving the cervix during a bimanual examination)
  • dizziness or syncope
  • shoulder tip pain (peritonitis - phrenic nerve)
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207
Q

What are the USS findings in an ectopic pregnancy?

A

Transvaginal USS
- gestational sac containing a yolk sac or fetal pole may be seen in a Fallopian tube

  • empty gestational sac
  • tubal ectopic = moves separately to the ovary
  • empty uterus
  • fluid in the uterus = pseudogestational sac

with BHCG >1500

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208
Q

What is a pregnancy of unknown location and how to investigate?

A

Positive pregnancy test but no evidence of pregnancy on USS

Track HCG:
1. rise >63% = intrauterine pregnancy
2. rise of <63% after 48 hrs/ stays the same = ectopic pregnancy
3. a fall >50% = miscarriage

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209
Q

What is the MC location of an ectopic pregnancy?

A
  1. Tubal ectopic

in ampulla

  • diagnosed by USS = adnexal mass that moves separately to the ovary
  • 20% of cases a pseudo sac seen within the uterine cavity
  • free fluid may be seen but no diagnostic
  • serum b-hCG should be performed
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210
Q

Management: Ectopic pregnancy

A

Perform pregnancy test in all women with abdominal or pelvic pain caused by ectopic pregnancy
–> referred to early pregnancy assessment unit

ectopic pregnancy must be terminated, it is not viable.

Terminating options:
1. expectant management (awaiting natural termination = needs no heart beat, HCG<1500, no significant pain)
2. Medical management (methotrexate)
3. Surgical management (salpingectomy (remove affected Fallopian tube) or salpingotomy (cut made in tube and ectopic pregnancy removed))

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211
Q

When is conservative management allowed in ectopic pregnancy?

A
  1. patient must be clinically stable and pain free
  2. have a tubal ectopic pregnancy <35mm with no visible heartbeat
  3. serum hCG <1000
  4. patient is able to return for follow up

repeat hCG on day 2,4 and

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212
Q

When is medical management allowed for ectopic pregnancy termination?

A

Systemic methotrexate

  1. have no significant pain and be clinically well
  2. enraptured tubal ectopic with an adnexal mass <35mm with no visible FH
  3. Serum hCG <1500
  4. Do not have an intrauterine pregnancy
  5. Can return for follow up
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213
Q

How is methotrexate used in pregnancy termination?

A

Methotrexate is highly teratogenic
- IM injection into a buttock
- halts progress of pregnancy
- advise not to get pregnant for 3 months after

bhCG monitored on day 4 + 7 and then weekly until hCG is negative

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214
Q

What are the contraindications of methotrexate?

A
  • thrombocytopenia
  • hepatic or renal dysfunction
  • immunocompromised
  • breastfeeding
  • peptic ulcer disease
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215
Q

When is surgical management advised for ectopic pregnancy?

A

First line in women who:
- have significant pain
- adnexal mass >35mm
- live ectopic
- HCG >5000
- signs of rupture
- haemodynamic instability

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216
Q

What are the options for surgical management in ectopic pregnancy?

A
  • laparoscopically preferred
    1. first line = salpingectomy
    (remove affected Fallopian tube)
    2. Salpingotomy
  • make incision in tube and remove ectopic pregnancy
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217
Q

Define: miscarriage types

A

Early miscarriage = 12 weeks gestation

late miscarriage = 12-24 weeks gestation

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218
Q

What is a missed, threatened, inevitable, and anembryonic miscarriage?

A

Missed miscarriage – the fetus is no longer alive, but no symptoms have occurred

Threatened miscarriage – vaginal bleeding with a closed cervix and a fetus that is alive

Inevitable miscarriage – vaginal bleeding with an open cervix

Anembryonic pregnancy – a gestational sac is present but contains no embryo

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219
Q

What is a complete miscarriage?

A

Complete miscarriage
– a full miscarriage has occurred,
- and there are no products of conception left in the uterus
- USS will show empty uterus
- present following an episode of PV bleeding

require bHCG follow up (still might be positive initially so need to come back)

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220
Q

What is an incomplete miscarriage?

A

Incomplete miscarriage
– retained products of conception remain in the uterus after the miscarriage
- USS = see mixed echoes within the uterine cavity
- in previous IUP seen, require bHCG monitoring to ensure failing IUP

<35 mm = expectant, medical or surgical management under LA
>35 mm = surgical or medical management in hospital

221
Q

What is a delayed miscarriage?

A

No symptoms
- diagnosed on transvaginal scan or booking scan at 12 weeks
(strict criteria so don’t miss just early pregnancy)

  1. requires visualisation of a gestation sac, yolk sac and foetal pole with a CRL >7mm with no foetal heart activity
  2. confirmed by 2nd sonographer
  3. if any doubt organised an USS in 1 week
222
Q

What is the management for delayed miscarriage?

A

CRL <22mm = expectant, medical or surgical

CRL <54mm = medical or surgical

CRL >54mm = medical treatment

consider signs/ symptoms of infection

223
Q

What are the USS findings in a miscarriage?

A

Transvaginal USS

  1. mean gestational sac diameter <25mm
  2. fetal pole and crown rump length <7mm
  3. no fetal heartbeat
224
Q

Management: miscarriage

A

less <6 weeks
- expectant management = wait for miscarriage
- repeat urine pregnancy test after 7-10 days

more than 6 weeks
1. early pregnancy assessment service

  1. USS = confirm location + viability
    - no fetal heartbeat (visible if CRL >7mm)
    - fetal pol should be visible of mean gestational sac diameter >25mm
  2. expectant management = 1-2 weeks to allow for miscarriage
  3. medical management
    - misoprostol = prostaglandin analogue (softens the cervix + stimulate contraction)
  4. Surgical management = manual/electric vacuum aspiration
    - prostaglandins
    - anti-rhesus D prophylaxis
225
Q

What are the legal requirements for termination of pregnancy?

A

Abortion is legal till 24 weeks

  • if continuing the pregnancy involves greater risk to the physical or mental of the women or existing children
  • 2 registered practitioners must sign
  • must be carried out by a registered medical practitioner in an NHS hospital or approved premise
226
Q

What is involved in a medical abortion?

A
  1. Mifepristone = anti-progesterone (halts pregnancy + relax cervix)
  2. Misoprostol = prostaglandin analogue 1-2 days later
    (softens cervix, stimulates contractions)
227
Q

What are the options for a surgical abortion?

A

Before surgery = cervical priming
- soften + dilate cervix
- misoprostol, mifepristone or osmotic dilators

  1. cervical dilatation + suction of the contents of the uterus (up to 14 weeks)
  2. cervical dilatation + evacuation using forceps (14-24 weeks)
228
Q

What is involved in post-abortion care?

A
  • symptoms = vaginal bleeding, abdo cramp up to 2 weeks
  • urine pregnancy test = 3 weeks
  • contraception discussed
  • support + counselling offered
229
Q

What are the types of multiple pregnancies?

A

Monozygotic: identical twins (from a single zygote)
Dizygotic: non-identical (from two differe=nt zygotes)
Monoamniotic: single amniotic sac
Diamniotic: two separate amniotic sacs
Monochorionic: share a single placenta
Dichorionic: two separate placentas

230
Q

How is a multiple pregnancy diagnosed and the type?

A

USS

  1. Dichorionic diamniotic twins = membrane between the twins, with a lambda sign or twin peak sign
  2. Monochorionic diamniotic twins = membrane between the twins, with a T sign
  3. Monochorionic monoamniotic twins = no membrane separating the twins

lambda sign or twin peak sign = triangular appearance where the membrane between the twins meets the chorion

T sign = where membrane between twins meets the chorion, single placenta

231
Q

Define: twin-twin transfusion syndrome

A
  • foetuses share a placenta
  • one fetus (recipient) receives the majority of the blood from the placenta + other (donor) is starved
  • recipient = fluid overload, heart failure, polyhydramnios
  • donor = growth restriction, anaemia, oligohydramnios

(laser treatment can destroy connection)

232
Q

Define: twin anaemia polycythaemia sequence

A

one twin becomes anemic whilst the other develops polycythaemia (raised Hb)

233
Q

What antenatal care is given to women with a multiple pregnancy?

A

Anaemia, FBC checked
- booking clinic
- 20 weeks
- 28 weeks

Additional scans for fatal growth, unequal growth
- 2 weekly sans from 16 weeks for monochorionic twins
- 4 weekly scan from 20 weeks for dichorionic twins

234
Q

What different delivery options are there for multiple pregnancies?

A

Monoamniotic twins require elective caesarean section at between 32 and 33 + 6 weeks.

Diamniotic twins (aim to deliver between 37 and 37 + 6 weeks):

  • Vaginal delivery = first baby has a cephalic presentation (head first)
  • Caesarean section = may be required for the second baby after successful birth of the first baby
  • Elective caesarean = is advised when the presenting twin is not cephalic presentation
235
Q

What are the types of diabetes in pregnancy?

A

Pre-existing
- type 1
- type 2
- cystic fibres related
- MODY - rare

Gestational diabetes
- true
- pre-existing diabetes presenting for the first time

236
Q
A
237
Q

Define: gestational diabetes

A

Diabetes triggered by pregnancy
- reduced insulin sensitivity during pregnancy that resolves after birth

238
Q

What are the risk factors for gestational diabetes?

A
  1. Previous gestational diabetes
  2. Previous macrosomic baby (≥ 4.5kg)
  3. BMI > 30
  4. Ethnic origin (black 5. Caribbean, Middle Eastern and South Asian)
  5. Family history of diabetes (first-degree relative
239
Q

What is the investigation for gestational diabetes?

A

Oral glucose tolerance test

  1. blood sugar measured (fasting)
  2. then drink 75g glucose drink
  3. blood sugar measure 2 hours later

fasting = <5.6 mol/l
at 2 hours = <7.8 mol/l

5- 6- 7- 8

240
Q

What signs would result in investigations for gestational diabetes?

A
  1. Large for dates foetus (macrosomia - big babies) >9. 5 lbs at birth
  2. Polyhydramnios = increased amniotic fluid
  3. Glucose on urine dipstick
241
Q

Management: Gestational diabetes

A
  1. fasting glucose <5.3mmol/l
    1 hour post meal <7.8
    - trial of diet and exercise for 1-2 weeks
    - metformin

OR fasting glucose >7mmol/l
- immediately start insulin +/- metformin
OR fasting glucose above 6mmol/l + macrosomia
- start insulin +/- metformin

  1. Insulin (if targets still not met)
  2. Glibenclamide (Sulfonylureas)
    - option for women who decline insulin or cannot tolerate metformin
242
Q

What is the importance of identifying GDM?

A
  • fetal macrosomia
  • increased risk of developing type 2 diabetes
  • some will have diabetes pre-dating the pregnancy
  • neonatal hypoglycaemia
  • perinatal mortality
  • should dystocia
  • birth related trauma
243
Q

What is the protocol for pregnancy with pre-existing diabetes?

A

Before pregnant:
- 5mg folic acid until 12 weeks gestation

Pregnancy:
- early dating and viability scan 7-9 weeks
- Aim for same targets
- use only insulin and metformin
- retinopathy screening at 28 weeks
- aspirin once daily from 12 weeks until delivery (reduce risk of pre-eclampsia)
- USS fetal growth scans at 28, 32, 36 weeks

Labour:
- advise planned delivery between 37-38 +6 weeks
- a sliding scale insulin regime = dextrose and insulin infusion titrate to blood sugar levels

244
Q

What is postnatal protocol for diabetes?

A

Gestational
- should resolve immediately after birth
- fasting glucose tested at 6 weeks
- advice on healthy lifestyle, contraception
- HbA1c at 13 weeks: 39-47 = high risk. >48 = type 2 diabetes
- annual HbA1c

Pre-existing
- lower their insulin doses
- insulin sensitivity will increase after birth and with breastfeeding

245
Q

What are babies of mothers with pre-existing diabetes at risk of?

A
  • neonatal hypoglycaemia
  • polycythaemia (raised Hb)
  • jaundice
  • congenital heart disease
  • cardiomyopathy
  • fetal macrosomia
  • respiratory distress syndrome
246
Q

What are the effects of pregnancy on diabetes?

A
  • increased insulin dose requirement
  • diabetic nephropathy may worsen
  • risk of progression/development of retinopathy due to rapid improvement in glycemic control
  • hypoglycaemia with relative hypo unawareness
  • diabetic ketoacidosis
247
Q

What is advised for the care of neonate from a diabetic mother?

A

Women with diabetes should feed their babies as soon as possible after birth (within 30 minutes) – reduce hypoglycaemia

Blood glucose testing routinely at 2 to 4 hours after birth in babies of women with diabetes

Minimum 24-hour hospital stay

248
Q

What hypertension medication should be stooped in pregnancy?

A

Cause congenital abnormalities
- ACE inhibitors e.g. ramipril
- Angiotensin receptor blockers e.g. losartan
- Thiazide and thiazide like diuretics e.g. indapamide

249
Q

Define: gestational hypertension

A

Hypertension occurring after 20 weeks gestation, without proteinuria

250
Q

Define: Pre-eclampsia

A

Pregnancy induced hypertension associated with organ damage, and PROTEINURIA

  • after 20 weeks –> when spiral arteritis of placenta form abnormally
  • leading to high vascular resistance
  1. hypertension >90/140
  2. significant proteinuria >300mg in 24 hrs
  3. > 20 weeks gestation (can occur in postpartum)
251
Q

What is the pathophysiology of pre-eclampsia?

A
  1. when the blastocyst implants on the endometrium - outer most layer called syncytiotrophoblast grows into endometrium
  2. chorionic villi form containing metal blood vessels
  3. trophoblast invasion of endometrium send signals to spiral arteries to reduce vascular resistance
  4. blood flow increases to these arteries and eventually they break down, leaving pools of blood called lacunae (20 weeks)
  5. maternal blood flows from uterine arteries into lacunae then back into uterine veins
  6. If lacunae formed inadequately –> high vascular resistance in spiral arteries + poor perfusion of placenta
  7. causes oxidative stress in placenta. releases inflammatory chemicals into systemic circulation -> systemic inflammation + impaired endothelial function
252
Q

What are the risk factors for pre-eclampsia?

A

High-risk factors are:

Pre-existing hypertension
Previous hypertension in pregnancy
Existing autoimmune conditions (e.g. systemic lupus erythematosus)
Diabetes
Chronic kidney disease

Moderate-risk factors are:

Older than 40
BMI > 35
More than 10 years since previous pregnancy
Multiple pregnancy
First pregnancy
Family history of pre-eclampsia

253
Q

What prophylaxis is given to high risk women for pre-eclampsia?

A

aspirin from 12 weeks

  • if have one high risk factor or more than one moderate risk factor
254
Q

What are the symptoms of severe pre-eclampsia?

A

Headache
Visual disturbance or blurriness
Nausea and vomiting
Upper abdominal or epigastric pain (this is due to liver swelling)
Oedema
Reduced urine output
Brisk reflexes + clonus
Papilloedema
Abnormal liver enzymes

255
Q

How to diagnose pre-eclampsia?

A

Systolic blood pressure above 140 mmHg
Diastolic blood pressure above 90 mmHg

PLUS any of:

  • Proteinuria (1+ or more on urine dipstick)
  • Organ dysfunction (e.g. raised creatinine, elevated liver enzymes, seizures, thrombocytopenia or haemolytic anaemia)
  • Placental dysfunction (e.g. fetal growth restriction or abnormal Doppler studies)

Proteinuria can be quantified using:

Urine protein:creatinine ratio (above 30mg/mmol is significant)
Urine albumin:creatinine ratio (above 8mg/mmol is significant)

256
Q

Management: pre-eclampsia

A
  • aspirin prophylaxis from 12 weeks
  • monitor BP
  • regular urine dipstick for proteinuria

Medical management of pre-eclampsia is with:

  1. Labetolol = first-line as an antihypertensive
  2. Nifedipine = (modified-release) is commonly used second-line (and if asthma contraindicates labetalol)
  3. Methyldopa = third-line (needs to be stopped within two days of birth)
  • Intravenous hydralazine = may be used as an antihypertensive in critical care in severe pre-eclampsia or eclampsia
  • IV magnesium sulphate = is given during labour and in the 24 hours afterwards to prevent seizures
  • Fluid restriction = is used during labour in severe pre-eclampsia or eclampsia, to avoid fluid overload (cerebral oedema)
257
Q

What is the management of pre-eclampsia post birth?

A

BP monitored closely

  1. Enalapril (1st line)
  2. Nifedipine or amlodipine
  3. Labetolol or atenolol
258
Q

Define: Eclampsia

A

Occurrence of one or more seizure in a woman with pre-eclampsia

  • seizure in a pregnant woman are always eclampsia until proven otherwise
  • increased risk in 24hrs after delivery
259
Q

Management: eclampsia

A
  1. IV magnesium sulphate
    - over 5 mins
    - followed by an infusion of 1g/hour maintained for 24 hrs
  2. stabilise mum first and then deliver baby
    (if give pregnant lady anaesthetic = cause cerebral haemorrhage)
260
Q

What can IV magnesium sulphate for eclampsia cause and treatment?

A

Respiratory depression
- calcium gluconate

261
Q

What is the HELLP syndrome?

A

Combination of features that occur as complications of pre-eclampsia + eclampsia

  1. Haemolysis
  2. Elevated Liver enzymes
  3. Low Platelets
262
Q

What causes anaemia during pregnancy?

A
  1. Plasma volume increase
  2. reduction in the haemoglobin concentration
  3. blood is diluted due to the higher plasma volume
263
Q

Presentation: Anaemia in pregnancy

A

Often anaemia in pregnancy is asymptomatic.

Women may have:

Shortness of breath
Fatigue
Dizziness
Pallor

264
Q

Investigations: anaemia in pregnancy

A

Booking bloods >110 g/l
28 weeks gestation >105 g/l
Postpartum >100 g/l

low MCV = iron deficiency
normal MCV = physiological anaemia due to increased plasma volume
high MCV = B12 or folate deficiency

Women are screened at the booking clinic for thalassaemia and sickle cell disease

265
Q

Management: anaemia in pregnancy

A
  1. Iron replacement e.g. ferrous sulphate
  2. B12 deficiency:
    - IM hydroxocobalamin injections
    - Oral cyanocobalamin tablets
  3. Folate deficiency
    - all women = 400mcg folic acid per day
    - deficiency = 5mg folic acid daily
266
Q

Why is VTE a risk in pregnancy?

A

thrombosis occurs as a result of stagnation of blood and hyper-coagulable states, such as pregnancy

PE is a significant cause of death in obstetrics
- highest in postpartum

267
Q

What are the risk factors for VTE in pregnancy?

A

Smoking
Parity ≥ 3
Age > 35 years
BMI > 30
Reduced mobility
Multiple pregnancy
Pre-eclampsia
Gross varicose veins
Immobility
Family history of VTE
Thrombophilia
IVF pregnancy

268
Q

What is the protocol for VTE prophylaxis in pregnancy?

A

1st trimester = 4 or more risk factors

at 28 weeks = if 3 risk factors

269
Q

Presentation: VTE in pregnancy

A

Unilateral
Calf or leg swelling
Dilated superficial veins
Tenderness to the calf (particularly over the deep veins)
Oedema
Colour changes to the leg

270
Q

Investigations: VTE in pregnancy

A
  1. Doppler USS

(well’s score not validated for pregnant women and pregnancy raises D-dimer naturally anyway)

PE
1. CXR
2. ECG
3. CT pulmonary angiogram CTPA

271
Q

Management: VTE in pregnancy

A

Prophylaxis
- Low molecular weight heparin e.g. Enoxaparin, Dalteparin, tinzaparin

Temporarily stopped in labour and then carried on 6 weeks postnatally (risk is higher in first 3 weeks postpartum)

PE
1. in fractionated heparin
2. thrombolysis
3. surgical embolectomy

272
Q

What are the complications of chickenpox in pregnancy?

A
  • More severe cases in the mother, such as varicella pneumonitis, hepatitis or encephalitis
  • Fetal varicella syndrome
  • Severe neonatal varicella infection (if infected around delivery)
273
Q

How to check exposure to chickenpox in pregnancy?

A
  • previously had chickenpox = they are safe
  • Not sure about their immunity = test the VZV IgG levels. If positive, they are safe.
  • Not immune = they can be treated with IV varicella immunoglobulins as prophylaxis against developing chickenpox. This should be given within ten days of exposure.
274
Q

Management: chickenpox in pregnancy

A
  1. oral aciclovir - if present within 24hrs and >20 weeks gestation
275
Q

Define: congenital varicella sundrome

A

occurs when infection occurs in first 28 weeks of gestation

Features:
- Fetal growth restriction
- Microcephaly, hydrocephalus and learning disability
- Scars and significant skin changes located in specific dermatomes
- Limb hypoplasia (underdeveloped limbs)
- Cataracts and inflammation in the eye (chorioretinitis)

276
Q

What is the risk of UTI in pregnancy?

A

Pregnant women are at higher risk of developing UTIs

Tested routinely for asymptomatic bacteriuria (bacteria present in urine)

277
Q

Presentation: UTI + pyelonephritis in pregnancy

A

Lower urinary tract infections present with:

Dysuria (pain, stinging or burning when passing urine)
Suprapubic pain or discomfort
Increased frequency of urination
Urgency
Incontinence
Haematuria

Pyelonephritis presents with:

Fever (more prominent than in lower urinary tract infections)
Loin, suprapubic or back pain (this may be bilateral or unilateral)
Looking and feeling generally unwell
Vomiting
Loss of appetite
Haematuria
Renal angle tenderness on examination

278
Q

Management: UTI in pregnancy

A

7 day course
1. nitrofurantoin (avoid in 3rd trimester)
2. Amoxicillin
3. Cefalexin

279
Q

Define: Oligohydramnios

A

Abnormally low volume of amniotic fluid surrounding the foetus during pregnancy

280
Q

What are the causes of Oligohydramnios?

A

Increase fluid loss or decreased fluid production

  • rupture of membranes
  • Fetal growth restriction
  • Maternal medical comorbidities (e.g. hypertension)
  • Placental abnormalities (e.g. abruption)
  • Fetal urinary tract anomalies (e.g. renal agenesis, posterior urethral valves)
  • Maternal drug use (e.g. NSAIDs, ACE inhibitors)
  • Post-term pregnancy
281
Q

Investigation: Oligohydaminos

A

USS
- no symptoms at all
- clear or light pink fluid leaking from vagina –> rupture of membranes

Examination
- fetal parts easier to feel
- uterus may appear small for dates
- sterile speculum examination

Fluid analysis
- ferrying test = cervical secretions, when dry should form a fern like pattern of crystals
- Amnisure = vaginal swab to screen for presence of placental alpha micro globulin-1 (high conc normally in amniotic fluid)
- Actim-PROM = swab that screens for insulin like growth factor binding protein-1 (high conc normally found in amniotic fluid)

282
Q

What is the diagnosis measurement of oligiohydramnios?

A

Amniotic fluid index <5cm
Maximum vertical pocket < 2cm

283
Q

Management: oligohydramnios

A
  1. Monitoring - serial fetal testing
  2. Intervention - therapeutic amino-fusion, saline or Ringer’s lactate is infused into the amniotic cavity
  3. time of delivery
    - induced labour 36-38 weeks
284
Q

What are some complications of oligohydramnios?

A
  • Pulmonary hypoplasia
  • limb deformities = due to fetal compression
  • porters labour
  • umbilical cord compression
  • meconium aspiration
  • caesarean delivery
  • non-reassuring fetal CTG traces
285
Q

Define: polyhydramnios

A

Abnormally large level of amniotic fluid during pregnancy
- above 95th centime for gestational age

286
Q

How should amniotic fluid vary during pregnancy?

A
  • Steadily increased until 33 weeks gestation
  • plateaus from 33-38 weeks and then declines
  • volume at term = 500ml
  • mainly comprised of fetal urine output
  • small bits of placenta and fetal secretions
  • foetus breathes and swallows amniotic fluid and then voided by the bladder
287
Q

What are the causes of polyhydramnios?

A
  • condition that prevents the foetus from swallowing
  • duodenal atresia ‘double bubble’
  • anaemia
  • fetal hydrops
  • twin to twin transfusion syndrome
  • increased lung secretions
  • maternal diabetes
  • maternal ingestion of lithium –> fetal diabetes insipidus
  • macrosomia - larger baby, more urine
  • infection
288
Q

Investigation: polyhydramnios

A
  1. palpate uterus - feel tense
  2. USS
    - assess fetal size, measure fluid volume
  3. maternal glucose tolerance test = maternal diabetes
  4. karyotyping - structural abnormalities
  5. TORCH infections = Toxicoplasmosis, Rubella, Cytomegalovirus, HSV
289
Q

Management: Polyhydramnios

A
  • no medical intervention usually required
  • Amnioreduction = if symptoms, associated with infection + placental abruption
  • Indomethacin = NSAID, enhance water retention, thus reduces fetal urine output
  • nasogastric tube = passed through baby to check for tracheoesophageal or oesophageal fistula
290
Q

What is the prognosis for polyhydramnios?

A

Usually good

complication
- postpartum haemorrhage = uterus has to contract further to achieve haemostasis
- cord prolapse
- malpresentation e.g. transverse lie, breech presentation

291
Q

Define: breech presentation + types

A

legs and bottom of foetus present first

Complete = legs are fully flexed at hips and knees

Incomplete = one leg flexed at the hip and extended at the knee

Extended = ‘frank breech’, both legs flexed at the hip and extended at the knee

Footling = foot is presenting through the cervix with leg extended

292
Q

Management: breech birth

A
  • turn spontaneously = babies before 36 weeks
  • external cephalic version = used at 37 weeks
  • can decide between vaginal birth or elective Caesarean section
293
Q

What is external cephalic version?

A

Technique used to turn a foetus from the breech position to a cephalic position using pressure on pregnant abdomen

  1. tocolysis = relax uterus
  2. subcutaneous terbutaline = beta agonist, reduces contractility of the myometrium

Rhesus-D negative women require anti-D prophylaxis when ECV performed

294
Q

define: stillbirth

A

birth of a dead foetus after 24 weeks gestation
- intrauterine fetal death

295
Q

What are the causes of stillbirth?

A

Unexplained (around 50%)
Pre-eclampsia
Placental abruption
Vasa praevia
Cord prolapse or wrapped around the fetal neck
Obstetric cholestasis
Diabetes
Thyroid disease
Infections, such as rubella, parvovirus and listeria
Genetic abnormalities or congenital malformations

296
Q

What increases the risk of stillbirth?

A

Fetal growth restriction
Smoking
Alcohol
Increased maternal age
Maternal obesity
Twins
Sleeping on the back (as opposed to either side)

297
Q

What prevention is taken to reduce likelihood of stillbirth?

A
  • risk assessment for baby small for gestational age
    or fetal growth restriction
  • serial growth scans to monitor fetal growth
298
Q

Management: stillbirth

A
  1. USS - confirm fetal heartbeat
  2. Rhesus D neg women require anti-D prophylaxis
  3. Vaginal birth (first line)
    - induction of labour
    - or expectant management awaiting natural labour
  4. Dopamine agonists = suppress lactation after stillbirth
  5. testing post birth with parental consent
299
Q

Define: cephalopelvic disproportion

A

Baby’s head doesn’t fit through the opening of your pelvis
- large babies
- out of position at birth canal
- shape of pelvis

300
Q

Management: cephalopelvic disproportion

A
  1. vacuum extraction or forceps
  2. Caesarean section
301
Q

What are complications of cephalopelvic disproportion?

A
  • baby’s shoulders might get stuck
  • require emergency c-section
  • vaginal tears
  • postpartum haemorrhage
302
Q

Define: uterine rupture

A

complication of labour = Muscle layer of the uterus ruptures

  • incomplete rupture or uterine dehiscence = uterine serosa surrounding the uterus remains intact
  • complete rupture = serosa ruptures along with the myometrium, contents of uterus released into peritoneal cavity
303
Q

What are the risk factors for uterine rupture?

A

Vaginal birth after caesarean (VBAC)
Previous uterine surgery
Increased BMI
High parity
Increased age
Induction of labour
Use of oxytocin to stimulate contractions

304
Q

Presentation: uterine rupture

A

Abdominal pain
Vaginal bleeding
Ceasing of uterine contractions
Hypotension
Tachycardia
Collapse

305
Q

Management: uterine rupture

A
  • obstetric emergency
  • resuscitation + transfusion may be required
  • emergency Caesarean section required to remove the baby, stop any bleeding and repair or remove uterus
306
Q

What the different types of ruptures of membranes?

A
  • Rupture of membranes = amniotic sac ruptured

Spontaneous rupture of membranes (SROM): The amniotic sac has ruptured spontaneously.

Prelabour rupture of membranes (PROM): The amniotic sac has ruptured before the onset of labour.

Preterm prelabour rupture of membranes (P‑PROM): The amniotic sac has ruptured before the onset of labour and before 37 weeks gestation (preterm).

Prolonged rupture of membranes (also PROM): The amniotic sac ruptures more than 18 hours before delivery.

307
Q

What are the levels of prematurity?

A

prematurity = before 37 weeks

<28 weeks = extreme preterm
28-32 weeks = very preterm
32-37 weeks = moderate to late preterm

308
Q

What are the 4 phases of cervical remodelling?

A

Softening = from early pregnancy

Ripening = weakness

Dilation = opening

Repair = after delivery

309
Q

What are the causes of preterm labour?

A
  1. Infection MC = from vagina, transplacental infection, peritoneal cavity, invasive procedures
  2. Placenta ischaemia = reduced blood flow to placenta
  3. uterine over distension = due to uterine abnormalities, polyhydramnios, multiple pregnancy
  4. Cervical weakness
    - primary cervical disease = congenital disorder. surgical trauma, interrupted structural integrity
    - secondary cervical insufficiency = 50% associated with infection
310
Q

What screening is done for preterm labour?

A

High risk
- previous preterm birth (biggest RF)
- previous cevical cerclage
- multiple pregnancy
- previous cervical treatment
- intrauterine adhesions
- uterine anomalies
- previous Caesarean section at full dilatation

High risk women then have cervical length measured
- using transvaginal USS
- cervical length <25mm between 16-24 weeks is associated with an increased risk of preterm birth

311
Q

What prophylaxis can be given for preterm labour?

A
  1. Vaginal progesterone gel or pessary = maintains pregnancy + prevent labour by decreasing activity of myometrium
    - for those with previous preterm labour or short cervix
  2. cervical cerclage =
    putting stitch in cervix to add support and keep it closed, removed when in labour
    - inserted around 11-14 weeks with history of 3 or more previous preterm birth
    - short cervix
    - or dilated preterm cervix
312
Q

Presentation: preterm labour

A

Abdominal pain
Vaginal/pelvic pressure
Increased vaginal discharge, bleeding, watery loss
Gastrointestinal disturbance
Urinary symptoms

Signs
- uterine contractions
- vulval changes = oedema, labial parting
- cervical changes
- liquor draining
- CTG changes
- maternal composition

313
Q

Assessment of someone in preterm labour

A

Uterine activity and cervical dilatation prior to 37 weeks

If uncertainty e.g. uterine activity without cervical dilatation:
< 30 weeks: Treat as threatened preterm labour
>30 weeks:
Fetal fibronectin
Cervical length (<15mm higher chance)
QUIPP app

314
Q

Management: preterm rupture of membranes

A
  1. prophylactic antibiotics = prevent development of chorioamnionitis
  2. induction of labour = from 34 weeks
315
Q

Investigation: preterm labour with intact membranes

A

Regular painful contraction + cervical dilatation, without rupture of amniotic sac

  • speculum exam
  • fatal fibronectin = glue between chorion and uterus, found in vagina during labour
316
Q

Management: preterm labour with intact membranes

A
  1. Fetal monitoring (CTG or intermittent auscultation)
  2. Tocolysis with nifedipine: nifedipine is a calcium channel blocker that suppresses labour
    (given at slow release so mothers BP doesn’t drop drastically)
  3. Maternal corticosteroids: can be offered before 35 weeks gestation to reduce neonatal morbidity and mortality
    - 2 IM injections 24 hrs apart
    - beneficial if baby is born 24-48hrs after 2nd dose given
  4. IV magnesium sulphate: can be given before 34 weeks gestation and helps protect the baby’s brain
    - prevents cerebral palsy
  5. Antibiotics
    - in labour to reduce risk of sepsis and cerebral palsy.
    - ideally given 4hrs before baby is born
317
Q

Non- pharmacological Management: of preterm babies

A
  1. Delayed cord clamping or cord milking: can increase the circulating blood volume and haemoglobin in the baby at birth
  2. thermoregulation
    - keep baby especially preterm babies warm
  3. Maternal early breast milk
    - use for mouth care
    - introduce baby to mothers microbiome
    - ask mother to start expressing some milk if know baby is going to be preterm
318
Q

Define: cord prolapse

A

When the umbilical cord descends below the presenting part of the fetus and through the cervix into the vagina, after rupture of the fetal membranes

319
Q

How to diagnose cord prolapse?

A

suspected where there are signs of fatal distress on the CTG
- diagnosed by vaginal examination or speculum exam

320
Q

Management: cord prolapse

A
  1. emergency caesarean section
    - reduce risk of cord compression + hypoxia to baby
    - cord should have minimal handling (cause vasospasm)
  2. woman lies in left lateral position (pillow under hip) or knee chest position (on all fours) - to reduce compression on cord
  3. Tocolytic medication = used to minimise contractions whilst waiting for delivery by caesarean section
321
Q

Define: instrumental delivery

A

refers to a vaginal delivery assisted by either a ventouse suction cup or forceps

322
Q

What are the indications for a instrumental delivery?

A

Failure to progress
Fetal distress
Maternal exhaustion
Control of the head in various fetal positions

(increased risk after epidural)

323
Q

What are the risks of a instrumental delivery?

A

Having an instrumental delivery increases the risk to the mother of:

Postpartum haemorrhage
Episiotomy
Perineal tears
Injury to the anal sphincter
Incontinence of the bladder or bowel
Nerve injury (obturator or femoral nerve)

The key risks to remember to the baby are:

Cephalohaematoma with ventouse
Facial nerve palsy with forceps

324
Q

What is a molar pregnancy?

A
  • type of gestational trophoblastic disease
    (can develop in to gestational cancer)

2 types:
1. complete mole = single sperm fertilising an egg which has lost its DNA (2-4% of developing into cancer)

  1. Partial = father supplies 2 sets of chromosome, but mothers chromosomes are also present (e.g. 2 sperm fertilising an egg so 3 sets of chromosomes)
325
Q

Investigation: molar pregnancy

A
  • diagnosed on USS = visualisation of an irregular echo bright area containing multiple cysts (bunch of grapes or snowstorm appearance)
326
Q

Management: molar pregnancy

A
  • only surgical = evacuation of contents of the uterus
  • increased risk of bleeding
  • send POC for urgent histology
  • may need chemo if metastasise
327
Q

What is antepartum haemorrhage?

A
  • bleeding from anywhere within the genital tract after the 24th week of pregnancy
  • occurs in 3-5 % pregnancies
328
Q

What are the causes of antepartum haemorrhage?

A

Identifiable causes:
Low Lying placenta / placenta praevia.= implanted into lower segment
Vasa praevia
Minor/Major abruption
Infection

329
Q

Management: low lying placenta

A

major - covering/reaching OS
minor - in lower segment/encroaching

diagnosed at 20 week anomaly USS

Management:
- Advise to present if pain / bleeding
- Advise to avoid sexual intercourse
- If recurrent bleeds may require admission until delivery and ensuring has cross-match in date
- Remember to give anti-D if Rh negative
- Elective LSCS around 37/40

330
Q

Management: bleeding placenta praevia

A
  • placenta covering os
  • ABCDE
  • if major bleed: two 14/16 G cannulas, IV fluids, X match 6 units, inform senior team and pads ASAP
  • examination abdominal, vaginal, USS
  • fetal monitoring
  • steroids if <34 weeks gestation
331
Q

What is vasa praevia?

A

Fetal vessels coursing through the membranes over the internal cervical os and below the fetal presenting part, unprotected by placental tissue or the umbilical cord

  • no major maternal risk, but major fetal risk
  • membrane rupture leads to major fetal haemorrhage
  • CTG abnormalities
332
Q

Define: morbidly adherent placenta or placenta accreta spectrum

A

placenta penetrates through the decides basalts and through the myometrium

333
Q

What are the types of placenta acreta?

A
  1. Superficial placenta accreta = is where the placenta implants in the surface of the myometrium, but not beyond
  2. Placenta increta = is where the placenta attaches deeply into the myometrium
  3. Placenta percreta = is where the placenta invades past the myometrium and perimetrium, potentially reaching other organs such as the bladder
334
Q

What are the risk factors for placenta accreta spectrum?

A

Previous placenta accreta
Previous endometrial curettage procedures (e.g. for miscarriage or abortion)
Previous caesarean section
Multigravida
Increased maternal age
Low-lying placenta or placenta praevia

335
Q

Presentation: placenta accreta spectrum

A
  • no symptoms
  • diagnosed on antenatal USS
  • or at birth when difficult to deliver placenta = postpartum haemorrhage
336
Q

Management: placenta accreta spectrum

A
  1. 20 w scan watch for anterior LLP is previous CS
    = loss of definition between wall of uterus and abnormal vasculature
  2. arrange elective CS at 36-37 weeks
    • may need hysterectomy, cell salvage
      - blood transfusion
      - intensive care for mother and baby
      - uterine preserving surgery
      - expectant management = leaving placenta in place to be reabsorbed over time
337
Q

Define: placental abruption

A
  • premature separation of the placenta from the uterine wall
  • concealed or revealed haemorrhage
338
Q

Presentation: placental abruption

A
  • woody hard abdomen
  • Sudden onset severe abdominal pain that is continuous
  • Vaginal bleeding (antepartum haemorrhage)
  • Shock (hypotension and tachycardia)
  • Abnormalities on the CTG indicating fetal distress
339
Q

What are the risk factors for placental abruption?

A
  • Advanced maternal age
  • previous placental abruption
  • smoker
  • cocaine use
  • multiple pregnancy
  • multigravida
  • trauma
  • pre-eclampsia
  • fetal growth restriction
340
Q

What is the severity of antepartum haemorrhage?

A

The RCOG guideline (2011) defines the severity of antepartum haemorrhage as:

Spotting: spots of blood noticed on underwear
Minor haemorrhage: less than 50ml blood loss
Major haemorrhage: 50 – 1000ml blood loss
Massive haemorrhage: more than 1000 ml blood loss, or signs of shock

341
Q

What are the 2 types of placental abruption?

A
  1. concealed = cervical os remained closed, bleeding occurs within uterine cavity
  2. revealed = blood loss is observed via the vagina
342
Q

Management: placental abruption

A
  1. Urgent involvement of a senior obstetrician, midwife and anaesthetist
    2 x grey cannula
    Bloods include FBC, UE, LFT and coagulation studies
    Crossmatch 4 units of blood
    Fluid and blood resuscitation as required
    CTG monitoring of the fetus
    Close monitoring of the mother
  2. emergency s-section
    - risk of postpartum haemorrhage
343
Q

What is the likelihood of sepsis on pregnancy?

A
  • sepsis is the leading cause of maternal death in the UK
  • advise all women to be immunised for seasonal flu and COVID
344
Q

What are the risk factors for sepsis in pregnancy?

A

Obesity
Diabetes
Impaired immunity /immunosuppressantmedication
Anaemia
Vaginal discharge
History of pelvic infection
History of group B Strepinfection
Amniocentesis and otherinvasive procedures
Cervical cerclage
Prolonged spontaneousrupture of membranes
Group A Strep infection inclose contacts / familymembers

345
Q

Management: sepsis

A

Timely recognition– be alert to signs/MEOWS

First hour SEPSIS SIX BUNDLE
1) O2 as required to achieve SpO2 over 94%
2) Take blood cultures
3) Commence IV antibiotics
4) Commence IV fluid resuscitation
5) Take blood for Hb,lactate(+glucose)
6)Measure hourly urine output

Ongoing multidisciplinary care: obstetrician, anaesthetist,critical care, microbiologist, etc

346
Q

Define: shoulder dystocia

A

failure for the anterior shoulder to pass under the symphysis pubis after delivery of the foetal head

347
Q

what are the risk factors for shoulder dystocia?

A

Macrosomia(most cases occur in normally grown babies)
Maternal diabetes
Previous shoulder dystocia
Disproportion between mother andfetus
Postmaturityand induction of labour
Maternal obesity
Prolonged 1stor 2ndstage of labour
Instrumental delivery

348
Q

Management: shoulder dystocia

A

H– Call forhelp(emergency buzzer)
E–Evaluate forepisiotomy
L–Legs in McRoberts
P– Suprapubicpressure
E–Enter pelvis
R–Rotational manoeuvres
R–Remove posterior arm
(R–Replace head and deliver by LSCS -Zavanelli)

349
Q

What are shoulder dystocia complications?

A

Maternal
PPH
Extensive vaginal tear(3rdand 4thdegree)
Psychological

Neonatal
Hypoxia
Fits
Cerebral palsy
Injury to brachial plexus

350
Q

What are the types of post partum haemorrhage?

A

Primary
- Within 24 hours of delivery, blood loss >500mls

Secondary
After 24 hours and up to 12 weeks post delivery

Minor(500 -1000mls)
Major(> 1000mls)

351
Q

What are the causes of post patrol haemorrhage?

A

The four ‘T’s
-Tissue: ensure placenta complete(MROP)
-Tone: ensure uterus contracted(uterotonics)
-Trauma: look for tears(repair)
-Thrombin: check clotting(transfusion RPC/ CP/FFP)

352
Q

What are the risk factors for postpartum haemorrhage?

A

Big baby
Nulliparity andgrandmultiparity
Multiple pregnancy
Precipitate orprolonged labour
Maternal pyrexia
Operative delivery
Shoulder dystocia
Previous PPH

353
Q

Investigations + management: secondary PPH

A

If haemodynamically unstable, resuscitate using an A to E approach
● Assess blood loss and full examination
● Send swabs - high vaginal swab (HVS) and
endocervical swab
● Pelvic ultrasound
● Manage according to likely cause
○ Antibiotics
○ Uterotonics if required (syntocinon)
○ Surgical measures if excessive or continuing
bleeding

354
Q

What are the causes of secondary PPH?

A
  • Endometritis (uterine infection)
    ● Retained placental fragments / tissue
    ● Abnormal involution of placental site
    ● Arteriovenous malformations
355
Q

What are the different hormonal contraceptions?

A

All release progesterone

  • combined pill
  • progesterone pill
  • implant
  • mirena coil
  • injection
356
Q

How often do smear tests occur?

A

25-64 yrs

25-50 yrs
Every 3 years

50-64 yrs
Every 5 years

357
Q

What is gravidity and parity?

A

gravidity - total number of pregnancies including current pregnancies
(gravida only if currently pregnant)

parity - total number of deliveries after 24 weeks
(is about past pregnancies, doesn’t matter if it was twins, stillbirth etc.)

Gravidity will always be higher as you are counting the current pregnancy

358
Q

How do you signify a pregnancy that has not gone beyond 24 weeks?

A

+1

e.g. P4 +1

359
Q

What pregnancy appointment are routine?

A

12 week booking clinic
- USS
- bloods for conditions
- dating scan
- sex

20 weeks
- USS
- position in uterus
- placental localisation
- foetal anatomy

37 weeks
- bloods
- check baby

360
Q

What are the different trimesters?

A

first trimester = till 12 weeks
second trimester = 12-28 weeks
full term = 37 weeks (till 42 weeks)

complete term = 40 weeks

361
Q

When should induction of labour be offered?

A

from 41 weeks if have not spontaneously gone into labour

362
Q

What are the stages of labour?

A
  1. Latent phase
    - contractions (may be irregular)
    - mucoid plugs (‘show’)
    - cervix is beginning to efface and dilate
    - last up to 2-3 days
  2. first stage
    - stronger uterine contractions
    - cervix is continuing to efface and dilate up to 10cm
  3. second stage
    - from full dilatation to the birth of the foetus
  4. third stage
    - from the birth of the foetus to the expulsion of the placenta
363
Q

What is the role of oxytocin in labour?

A

A surge in oxytocin levels at the onset of labour will contract the uterus

364
Q

What is the role of prostaglandins in labour?

A

To aid with cervical ripening

365
Q

What is the role of prolactin?

A

to begin the process of milk production in the mammary glands

366
Q

What is the role of oestrogen in labour?

A

surges at the onset of labour to inhibit progesterone to prepare the smooth muscles for labour

367
Q

What is the role of beta-endorphins?

A

natural pain relief in labour

368
Q

What is the role of adrenaline in labour?

A

released as birth is imminent to give the woman the energy to give birth

369
Q

Where do contractions occur and what is happening?

A
  • Starts in the fundus (pacemaker)
  • Retraction/shortening of muscle fibres
  • Build in amplitude as labour progresses
  • Fetus forced down causing pressure on cervix
370
Q

What is effacement?

A

Cervical effacement (also called cervical ripening) refers to a thinning of the cervix.

  • Prior to effacement, the cervix is like a long bottleneck, usually up to 4cm in length.
  • Throughout pregnancy, the cervix is tightly closed and protected by a plug of mucus.
  • in labour cervix shortens
  • midwives do a sweep of the cervix to release the bodies natural hormones
371
Q

What is the most common type of female pelvis?

A

Gynaecoid MC
- The inlet is slightly transverse oval
Sacrum is wide with average concavity and inclination
Side walls are straight with blunt ischial spines
Wide subpubic arch

372
Q

What are the steps in the foetal journey of birth?

A
  1. Descent
  2. Flexion
  3. Internal rotation
  4. Extension
  5. Restitution - baby turns to allow shoulders to get out
  6. External rotation
  7. Delivery of body
373
Q

What happens in descent?

A

The fetus descends into the pelvis

This can occur from 37 weeks gestation onwards, and may not occur until established labour.

It is encouraged by:
- Increased abdominal muscle tone
- Increased frequency and strength of contractions

374
Q

What happens in flexion step of labour?

A
  1. as fetus descends through the pelvis, uterine contractions exerts pressure down the fetal spine towards the occiput, forcing the occiput to come into contact with the pelvic floor.
  2. When this occurs, the fetal neck flexes allowing the circumference of the fetal head to reduce.
  3. In this position, the fetal skull has a smaller diameter which assists passage through the pelvis.
375
Q

What occurs during the internal rotations step of labour?

A
  1. With each maternal contraction, the fetal head pushes down on the pelvic floor.
  2. Following eachcontraction, a rebound effect supports a small degree of rotation.
  3. Regular contractions eventually lead to the fetal head completing the 90-degree turn.
376
Q

What occurs during there extension step of labour?

A
  1. The foetal occiput slips beneath the suprapubic arch allowing the head to extend.
  2. The fetal head is now born and will be facing the maternal back with its occiput anterior.
377
Q

What occurs during the restitution/external rotation step of the labour?

A
  1. the shoulders at the point of the head being delivered are only just reaching the pelvic floor they are often still negotiating the pelvic outlet and the fetus may naturally align its head with the shoulders.
  2. visually you may see the head externally rotate to face the right or left medial thigh of the mother
378
Q

What occurs in the delivery step of labour?

A
  1. Gentle downward traction may be conducted by the midwife to assist with the delivery of the shoulder below the suprapubic arch.
  2. This then may be followed by gentle upwards traction assisting the delivery of the posterior shoulder.
379
Q

Define: En cal

A

when a baby is born within the amniotic sac

380
Q

What is delayed cord clamping and benefits?

A
  • Delayed cord clamping is the practice in which the umbilical cord is not immediately clamped and cut at the point of birth, but allowed at least 1 minute to transfuse blood to the baby.
  • The baby could receive up to 214g of blood if this is facilitated.

Associated benefits:
- Allows the baby time to transition to extra-uterine life
- Increase in red blood cells, iron and stem cells (this can aid with growth and development up to 6 months old)
- Reduced need for inotropic support

381
Q

What is the placenta?

A
  • temporary organ during pregnancy = made up of lobes attached to the uterine wall
  • connected t the foetus via the umbilical cord which ahas 2 arteries and one vein
  • produced hormones that assist with fetal growth

In
- oxygen and nutrients
- (alcohol + nicotine)
- maternal antibodies

out
- waste products e.g. CO2
- passed back to maternal blood stream for disposal

382
Q

What are the 2 membranes of the placenta?

A

amnion = bag around baby
chorion = membrane around placenta

383
Q

What are the options for birth positions?

A
  1. immersion in water
    - reduced pain
    - analgesia aspects
    - promotes calmness
    - hands off approach
  2. upright birth
    - increases diameter the pelvic inlet
    - less risk of compressing mothers aorta
    - encourages stronger and longer contractions
    - gravity
384
Q

What holistic non invasive analgesia can be used in birth?

A

Water immersion (birthing pool or bath)
Aromatherepy
Massage
Hypnobirthing
TENS machine
Entonox (gas and air)
paracetamol
codeine

385
Q

What opioid options are there in labour?

A

Diamorphine
Pethidine
Remifentanyl

386
Q

How does epidural work? pros and cons?

A
  • Epidural analgesia is a mixture of bupivacaine and fentanyl
  • Epidural catheter is inserted by an anaesthetist, and drugs are administered through this via a pump.

pros:
Total pain relief in 90% of cases
Effect will last until the baby is born

Cons:
Reduced mobility
Can take up to an hour to take effect
Will need a urinary catheter
Can slow down labour if not established

387
Q

What asymptomatic screening is offered for females and heterosexual males?

A

Female
Self taken Vulvo-vaginal swab for Gonorrhoea/Chlamydia NAAT (Nucleic Acid Amplification Test)
Bld for STS + HIV

Heterosexual male
First void urine for Chlamydia/Gonorrhoea NAAT
Bld test for STS + HIV

388
Q

What asymptomatic screening is offered to gay men?

A

MSM (Men who have Sex with Men):
First void urine for Chlamydia/Gonorrhoea NAAT
Pharyngeal swab for Chlamydia/Gonorrhoea NAAT (may be self taken)
Rectal swab for Chlamydia/Gonorrhoea NAAT (may be self taken)
Bld for STS, HIV, Hep B (& Hep C if indicated

389
Q

What symptoms would a female with an STI present with?

A

Vaginal discharge

Vulval discomfort/soreness, itching or pain

Superficial dyspaerunia

Pelvic pain/deep dyspaeruniaVulval lumps

Vulval ulcers

Inter-menstrual bleeding

Post-coital bleeding

390
Q

What is the symptomatic presentation for men with STIs?

A

Pain/burning during micturition

Pain/discomfort in the urethra

Urethral discharge

Genital ulcers, sores, or blisters

Genital lumps

Rash on penis or genital area

Testicular pain/swelling

391
Q

Who is screened for hepatitis B?

A

Men who have Sex with Men (MSM)
Commercial Sex Workers (CSW) and their sexual partners
IVDUs (current or past), and their sexual partners
People from high risk areas and their sexual partners
Africa, Asia, Eastern Europe

Aim to vaccinate them if non-immune

392
Q

What treatment is offered to partners?

A

Central activity in GUM

Necessary to prevent re-infection of index patient

To identify & treat asymptomatic infected individuals as a public health measure

Role of Health advisers

Importance of confidentiality in maintaining patient trust

393
Q

Define: PEP and PREP

A

PEP = post exposure prophylaxis (antiretorviral)

PREP = pre exposure prophylaxis (given in anticipation of exposure to HIV)

394
Q

What are the options for inducing labour?

A
  1. membrane sweep = involves inserting a finger into the cervix to stimulate the cervix
  2. vaginal prostaglandin E2 = inserting gel, tablet, or pessary into the vagina, stimulating the cervix
  3. cervical ripening balloon = silicon balloon inserted into cervix + gently inflated to dilate the cervix
  4. artificial rupture of membranes = oxytocin infusion
  5. oral mifepristone + misoprostol = used when intrauterine fetal death has occurred
395
Q

What monitoring is used during induction of labour?

A
  1. Cardiotocography (CTG) = to assess fetal heart rate and uterine contractions before and during induction of labour
  2. Bishop score
396
Q

What scoring system is used to determine whether to induce labour?

A

Bishop Score

Fetal station (scored 0 – 3)
Cervical position (scored 0 – 2)
Cervical dilatation (scored 0 – 3)
Cervical effacement (scored 0 – 3)
Cervical consistency (scored 0 – 2)

397
Q

Define: uterine hyperstimulation

A
  • main complication of induction of labour with vaginal prostaglandins
  • contractions are prolonged and frequent causing fetal distress and compromise

Criteria
1. Individual uterine contractions lasting more than 2 minutes in duration
2. More than five uterine contractions every 10 minutes

398
Q

Management: uterine hyperstimulation

A
  • removing the vaginal prostaglandins or stopping the oxytocin infusion
  • tocolysis with terbutaline
399
Q

What are the complications of uterine hyper stimulation?

A
  • fetal compromise with hypoxia and acidosis
  • emergency Caesarean section
  • uterine rupture
400
Q

What are the 3 things progress in labour is influenced by?

A
  1. power = uterine contractions
  2. passenger = size, presentation, and position of the baby
  3. passage = the shape and size fo the pelvis and soft tissue
401
Q

What is the criteria for delay in the 1st stage of labour?

A

Less than 2cm of cervical dilatation in 4 hours

Slowing of progress in a multiparous women

402
Q

Management: failure to progress

A

Amniotomy, also known as artificial rupture of membranes (ARM) for women with intact membranes
Oxytocin infusion
Instrumental delivery
Caesarean section

403
Q

When are perineal tears more common?

A

First births (nulliparity)
Large babies (over 4kg)
Shoulder dystocia
Asian ethnicity
Occipito-posterior position
Instrumental deliveries

404
Q

What is the classification for perineal tears?

A
  1. First-degree – vaginal mucosa torn
  2. Second-degree – perineal muscles torn
  3. Third-degree – including the anal sphincter:
    - 3a = <50% of external anal sphincter affected
    - 3b = >50% of external anal sphincter affected
    - 3c = external and internal anal sphincter affected
  4. Fourth-degree – rectal mucosa torn
405
Q

Management: perineal tears

A

1st degree - no sutures
2nd degree + = sutures
3rd + 4th degree = repairing in theatre

Additional measures are taken to reduce the risk of complications:

  • Broad-spectrum antibiotics = to reduce the risk of infection
  • Laxatives = to reduce the risk of constipation and wound dehiscence
  • Physiotherapy = to reduce the risk and severity of incontinence
  • Followup = to monitor for longstanding complications
406
Q
A
407
Q

What is an episiotomy?

A

when the obstetrician or midwife cuts the perineum before the baby is delivered

  • cut made diagonally from the opening of the vagina downwards and laterally, to avoid damaging the anal sphincter = mediolateral episiotomy
408
Q

What physiological changes occur in pregnancy?

A

Hormones
Increase production of:
- ACTH = increase cortisol + aldosterone lead to improvement in most autoimmune conditions and more susceptible to diabetes and infections
- prolactin
- melanocyte = increase pigmentation
- T3 + T4
- Progesterone + oestrogen = vaginal hypertrophy

Cardiovascular:
- increased blood volume, plasma volume, cardiac output
- decreased peripheral vascular resistance, blood pressure

respiratory
- increased tidal volume and respiratory rate

Renal
- increased blood flow to kidneys, GFR, aldosterone (increase salt + water retention), protein excretion

Blood
- increased WBC, Esr, ALP, RBC (so higher iron, folate and B12 requirements)

409
Q

What are the implications of STIs for pregnancy?

A

Implications for management of pregnancy:
- HIV - Viral load, compliance with medication
- Vertical transmission of all infections
- Associations with miscarriage, fetal growth restriction, preterm birth and neonatal sepsis

Doxycycline = contraindicated in pregnancy

410
Q

What emergency contraception options are there?

A
  1. levonorgestrel (progesterone only pill) = 72 hrs
  2. copper IUD = up till 5 days
  3. ulipristal acetate (selective progesterone receptor modulator) = 120 hrs
411
Q

Define: vaginismus

A

Involuntary spasming of vaginal muscles

412
Q

Define: vulvodynia

A

unnatural pain response when anything touches the vulva

413
Q

What are indications for mammography?

A
  • Clinically suspicious lump in patients > 40 years
  • Breast cancer where mammography not previously performed [any age]
  • Residual lump after cyst aspiration
  • Single duct blood stained nipple discharge
  • Nipple skin change
  • Triennial mammograms between ages 47 and 73 as part of the National Breast Screening Programme.
  • breast cancer
  • increased familial risk aged 40-50 yrs
414
Q

What are contraindications to mammography?

A
  • breast pain without a lump
  • symmetrical thickening
  • before commencing HRT
  • women under 40 years unless diagnosed with previous breast cancer.
415
Q

Investigations: breast lumps

A

Clinical examination

< 24 yrs = USS

25-39 yrs = USS + histology or cytology

> 40 yrs = mammography + USS and either histology or cytology

416
Q

Presentation: lumps in breast cancer

A
  • Lumps that are hard, irregular, painless or fixed in place
  • Lumps may be tethered to the skin or the chest wall
  • Nipple retraction
  • nipple discharge
  • Skin dimpling or oedema (peau d’orange)
  • lymphadenopathy
417
Q

When is the 2 week referral recommended for breast cancer?

A
  • unexplained breast lump in patients > 30 years
  • unilateral nipple changes in patients >50 yrs
  • unexplained lump in axilla in patients > 30 yrs
  • skin changes suggestive of breast cancer
418
Q

What is the triple assessment?

A

Done for every woman with a complaint of breast lumps

  1. History + examination
  2. Imaging - mammogram (over 40yrs) or MRI (any age)
  3. biopsy
419
Q

Why is a mammogram better than a USS?

A

Looks at the whole breast
compares both breasts

USS - just looks at the focal abnormality
(used in women <49 yrs as breast tissue is to dense for a mammogram - glandular and cancerous tissue both appear white on scan)

420
Q

What criteria defined breast cysts as non-cancerous?

A

when fluid is aspirated:
- the fluid is not blood stained
- there is no residual lump
- the cyst does not continually refill

421
Q

When is chemo used in breast cancer before surgery?

A

First test for receptors (oestrogen, progesterone, HER2)

chemo effective for:
- HER 2 positive
- Triple negative (as won’t respond to hormones)
- inflammatory breast cancer
- a large cancer

also can shrink tumour so breast conservation surgery can happen

Converts inoperable to operable disease in the breast or axilla

422
Q

When is chemo used for breast cancer after surgery?

A
  • cancer cells found in lymph nodes
  • cancer cells don’t have hormone receptors
  • breast cancer cell are high grade >3
  • small HER2 positive breast cancer
423
Q

What is done for young women having chemo for breast cancer?

A

Egg collection and embryo freezing

  • check for gene testing
424
Q

How does lymph node assessment work for breast cancer?

A
  • assess to see if cancer has spread to lymph nodes
  • USS of axilla and guided biopsy

sentinel lymph node biopsy
- performed during breast surgery
- an isotope contrast and blue dye are injected into the tumour area
- lymph nodes can then be removed or biopsied

425
Q

What are the types of breast cancer receptors?

A
  1. Oestrogen receptors (ER)
  2. Progesterone receptors (PR)
  3. Human epidermal growth factor (HER2)

Triple-negative breast cancer
= is where the breast cancer cells do not express any of these three receptors. This carries a worse prognosis, as it limits the treatment options for targeting the cancer.

426
Q

Where can breast cancer metastasis to?

A

Lungs
Liver
Bones
Brain
2Ls and 2 Bs

but it can spread practically everywhere

427
Q

What are the surgery options for breast cancer?

A

tumour removal:
1. lumpectomies
(if less than <20% of breast tissue needs to be removed)

  1. mastectomy
    (multiple tumours, big tumours, when radiotherapy is contraindicated (for previous breast cancer or for lymphoma), advanced disease, patient choice)

Similar survival rates

Axillary clearance
- removal of axillary lymph nodes

428
Q

What is a complication of lymph node clearance?

A

chronic lymphoedema
- buildup of fluid in an arm

429
Q

What is the management for chronic lymphedema?

A

Massage techniques to manually drain the lymphatic system (manual lymphatic drainage)
Compression bandages
Specific lymphoedema exercises to improve lymph drainage
Weight loss if overweight
Good skin care

430
Q

What are non-surgical management options for breast cancer?

A
  1. radiotherapy
    - used in patients after breast conserving surgery to reduce risk of recurrence
  2. chemo
    - neoadjuvant = shrink tumour before surgery
    - adjuvant = given after surgery to reduce recurrence
    - treatment
  3. hormones
    - Tamoxifen = premenopausal women (blocks oestrogen receptors in ER positive cancers)
    - aromatase inhibitors = postmenopausal women, block the creation of oestrogen in fat tissue
431
Q

What hormonal treatment is used used for HER2 receptors?

A
  1. Trastuzumab (Herceptin) = monoclonal antibody that targets HER2 receptor
  2. Pertuzumab (perjeta) = monoclonal antibody targets HER2 receptors
  3. Neratinib (nerlynx) = tyrosine kinase inhibitor, reducing the growth of breast cancers
432
Q

What is the difference between grade and stage in cancers?

A

Grade = how different the cells look down the microscope from the original cell

Stage = how advanced and spread the cancer is

433
Q

Define: fibroadenoma

A

common benign tumours of stromal/epithelial breast duct tissue

  • common in younger women aged 20-40 yrs
  • respond to female hormones so often regress in menopause
434
Q

Presentation: fibroadenomas

A
  • painless
  • Smooth
  • Round
  • Well circumscribed (well-defined borders)
  • Firm
  • Mobile (moves freely under the skin and above the chest wall)
  • Usually up to 3cm diameter
435
Q

Define: fibrocystic breast changes

A
  • generalised lumpiness to the breast
  • normal variation
  • fluctuate with menstrual cycle
  • great pain or tenderness
  • fluctuation of breast size
436
Q

Management: fibrocystic breast changes

A
  • Wearing a supportive bra
  • Non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen
  • Avoiding caffeine is commonly recommended
  • Applying heat to the area
  • Hormonal treatments (e.g., danazol and tamoxifen) under specialist guidance
437
Q

Presentation: breast cysts

A

Benign, individual, fluid filled lumps
- smooth
- well circumscribed
mobile
- possibly fluctuate
- ages 30-50 yrs

438
Q

Investigations: breast cysts

A
  • imaging
  • aspiration or excision
    (aspiration can resolve pain)
439
Q

Define: fat necrosis

A

Benign lump formed by localised degeneration and scarring of fat tissue in the breast
- associated with an oil cysts containing liquid fat

440
Q

presentation: fat necrosis

A

Fat necrosis causes a benign lump formed by localised degeneration and scarring of fat tissue (MC by trauma, radiotherapy or surgery)

Painless
Firm
Irregular
Fixed in local structures
There may be skin dimpling or nipple inversion

441
Q

Management: fat necrosis

A
  • USS
  • Mammogram
    similar appearance to breast cancer
  • histology = fine needle aspiration or core biopsy
    (helps exclude breast cancer)
442
Q

Define: Lipoma

A

benign tumours of fat adipose tissue
- can occur anywhere in the body
- soft
- painless
- mobile
- do not cause skin changes

treated conservatively but can be surgically removed

443
Q

Define: Galactocele

A

Occur in lactating women, often after stopping breastfeeding
- breast milk filled cysts (lactiferous duct is blocked)
- firm
- mobile
- painless
- usually beneath the areola

usually resolve without treatment

444
Q

Define: Phyllodes tumour

A

Rare tumours of connective tissue of the breast
- ages 40-50 yrs
- large and fast growing
- can be benign or malignant and metastasis
- surgical removal,
- chemo

445
Q

What are the risk factors for breast cancer?

A

Female (99% of breast cancers)
Increased oestrogen exposure (earlier onset of periods and later menopause)
More dense breast tissue (more glandular tissue)
Obesity
Smoking
Drinking
Having less children and older
Family history (first-degree relatives)

Combined contraceptive pill (increase slightly but decreases after having stopped for 10 yrs)
HRT

446
Q

What are the types of breast cancer?

A
  1. ductal carcinoma in situ
  2. lobular carcinoma in situ
  3. Invasive ductal or carcinoma
  4. Invasive lobular carcinomas
  5. inflammatory breast cancer
  6. Paget’s disease of the nipple
447
Q

Presentation: ductal carcinoma in situ

A
  • Pre-cancerous or cancerous epithelial cells of the breast ducts
  • Localised to a single area
  • Often picked up by mammogram screening
  • Potential to spread locally over years
  • Potential to become an invasive breast cancer (around 30%)
  • usually complete mastectomy
  • Good prognosis if full excised and adjuvant treatment is used
448
Q

What are the features of lobular carcinoma in situ?

A
  • A pre-cancerous condition occurring typically in pre-menopausal women
  • Usually asymptomatic and undetectable on a mammogram
  • Usually diagnosed incidentally on a breast biopsy
  • Represents an increased risk of invasive breast cancer in the future (around 30%)
  • Often managed with close monitoring (e.g., 6 monthly examination and yearly mammograms)
449
Q

What are the features of Paget’s disease of the nipple?

A
  • Looks like eczema of the nipple/areolar
  • Erythematous, scaly rash
  • Indicates breast cancer involving the nipple
  • May represent DCIS or invasive breast cancer
  • Requires biopsy, staging and treatment, as with any other invasive breast cancer
450
Q

What is peau d’orange?

A

Orange bumpy discolouring of the breast
- usually signified in inflammatory breast cancer
- start with chemotherapy
(to kill cancer in lymphatics)
- and then operate

very bad prognosis

450
Q

age

A
451
Q

What are the guidelines for breast screening?

A

women ages 50 to 70 = every 3 years

MRI screening for BRCA gee carriers from aged 30 yrs

452
Q

What is the guidelines for breast screening for people with familial risk?

A
  • A first-degree relative with breast cancer under 40 years
  • A first-degree male relative with breast cancer
  • A first-degree relative with bilateral breast cancer, first diagnosed under 50 years
  • Two first-degree relatives with breast cancer
453
Q

Define + types: breast abscess

A

collection of pus within an area of the breast usually caused by a bacterial infection

  1. lactational abscess
    - associated with breastfeeding
    - Mastitis can lead to abscess
  2. non-lactational abscess
    - unrelated to breastfeeding
454
Q

What are the most common causative bacterial of breast abscesses?

A
  1. Staphylococcus aureus (the most common)
  2. Streptococcal species
  3. Enterococcal species
  4. Anaerobic bacteria (such as 5. Bacteroides species and anaerobic streptococci)
455
Q

Presentation: breast abscess

A

Mastitis with infection in the breast tissue presents with breast changes of:

Acute onset
Nipple changes
Purulent nipple discharge (pus from the nipple)
Tender fluctuant lump
Localised pain
Tenderness
Warmth
Erythema (redness)
Hardening of the skin or breast tissue
Swelling

456
Q

Management: breast abscess

A

lactational mastitis
- continued breastfeeding
- expressing milk
- breast massage
- heat packs
- warm showers
- simple analgesia
- antibiotics = flucloxacillin

non-lactational mastitis
- analgesia
- antibiotics
- treatment of underlying cause e.g. eczema, candidly infection

breast abscess
- antibiotics
- USS
- drainage = needle aspiration
- microscopy, culture and sensitivities of fluid

457
Q

define: intra ductal papilloma

A

wart lesion that grows within one of the ducts in the breast
- result of proliferation of epithelial cells
- benign tumours
- can be associated with atypical hyperplasia or breast cancer

458
Q

presentation: papilloma

A

often asymptomatic
- accidentally picked up on mammograms

present with:
- Nipple discharge (clear or blood-stained)
- Tenderness or pain
- A palpable lump

459
Q

Diagnosis: papilloma

A

Patients require triple assessment with:

  1. Clinical assessment (history and examination)
  2. Imaging (ultrasound, mammography and MRI)
  3. Histology (usually by core biopsy or vacuum-assisted biopsy)

ductography = inject contrast into abnormal duct and perform mammograms to visualise duct (papilloma an area that doesn’t fill with contrast)

460
Q

Management: papilloma

A

Complete surgical excision
- tissue then examined for atypical hyperplasia or cancer

461
Q

Define: ductal ectasia /

A

Benign breast condition
- as menopause approaches women’s nipples shorten and widen
- fluid can collect in the widened ducts

462
Q

Presentation: duct ectasia

A
  • Discharge from the nipple – usually thick but sometimes watery and may be brown, green or bloodstained
  • Breast pain = not common
  • A lump felt behind the nipple – this could mean the tissue behind the nipple has become infected or scarred
  • The nipple can be red or tender
  • The nipple is pulled inwards (inverted) – this could be because the ducts have shortened

MC in middle aged women

463
Q

How do you diagnose duct ectasia?

A
  • breast examination
  • mammogram
  • USS
  • core biopsy of breast
  • fine needle aspiration
464
Q

Management: duct ectasia

A
  • most don’t need treatment (normal part of ageing)
  • analgesia for pain
  • if infected = antibiotics
  • surgery if discharge continues = remove affected ducts
465
Q

What are the causes of small for gestational age?

A
  1. Constitutionally small, matching the mother and others in the family, and growing appropriately on the growth chart
  2. Fetal growth restriction (FGR), also known as intrauterine growth restriction (IUGR)
    - placental mediated growth restriction e.g. smoking, alcohol, malnutrition, anaemia, infection
    - non-placental mediated growth restriction e.g. genetic/structural abnormalities, fetal infection, errors of metabolism
466
Q

What are the complications of SGA?

A

Fetal death or stillbirth
Birth asphyxia
Neonatal hypothermia
Neonatal hypoglycaemia

long term risk of: Cardiovascular disease, particularly hypertension
Type 2 diabetes
Obesity
Mood and behavioural problems

467
Q

What are risk factors for SGA?

A

Previous SGA baby
Obesity
Smoking
Diabetes
Existing hypertension
Pre-eclampsia
Older mother (over 35 years)
Multiple pregnancy
Low pregnancy‑associated plasma protein‑A (PAPPA)
Antepartum haemorrhage
Antiphospholipid syndrome

468
Q

Management: small for gestational age

A
  1. identifying those at risk
  2. aspirin = if at risk of pre-eclampsia
  3. treat modifiable risk factors = stop smoking
  4. serial growth scan
  5. early delivery where growth is static
  • blood pressure + urine dipstick
  • uterine artery doppler scanning
  • detailed fetal anatomy scan
  • karyotyping
  • test for infections
469
Q

Define + causes: macrosomia

A

Constitutional
Maternal diabetes
Previous macrosomia
Maternal obesity or rapid weight gain
Overdue
Male baby

470
Q

What are the risks of macrosomia?

A

The risks to the mother include:

Shoulder dystocia
Failure to progress
Perineal tears
Instrumental delivery or caesarean
Postpartum haemorrhage
Uterine rupture (rare)

The risks to the baby include:

Birth injury (Erbs palsy, clavicular fracture, fetal distress and hypoxia)
Neonatal hypoglycaemia
Obesity in childhood and later life
Type 2 diabetes in adulthood

471
Q

Management: Macrosomia

A
  • Ultrasound to exclude polyhydramnios and estimate the fetal weight
  • Oral glucose tolerance test for gestational diabetes

can still have vaginal delivery = just higher risk for shoulder dystocia

472
Q

What are the different symptoms for ovarian, endometrial, cervical, vaginal and vulva cancer?

A

cervical
- smears pick up HPV

Endometrial
- post-menopausal bleed
- haematuria visible
- thrombocytosis
- vaginal discharge unexplained

Ovarian
- appetite loss or early satiety
- abdominal distension
- ascites
- abdominal/pelvic mass
- abdominal/pelvic pain
- IBS symptoms
- change in bowel habit
- fatigue
- urinary urgency
- weight loss
- serum CA125 results

Vaginal
- mass in or at entrance to the vagina

Vulva
- vulval bleeding
- vulval lump or ulceration

473
Q

What are the gynaecologist tumour markers?

A
  • CA 125 (only use for post-menopausal)
  • beta-HCG (high when not pregnant)
  • alpha fetoprotein
  • Inhibin (normally produced by ovarian granuloma cells - ovarian tumours)
  • carcinoembryonic antigen CEA
474
Q

What is included under the 2 week wait criteria?

A
  • post-menopausal bleeding

Transvaginal USS for women over 55 yrs with:
- unexplained vaginal discharge
- visible haematuria plus raised platelets, anaemia or elevated glucose levels

475
Q

Define: chronic pelvic pain

A

intermittent or constant pain in the pelvic area for at least 6 months
- not exclusively related to menstruation, intercourse or pregnancy

476
Q

Which swab is used for each infection?

A

High vaginal swabs = candida, bacterial vaginosis, trichomonad

Endocervical = Gonorrhoea, chlamydia

Cervical smear = HPV

477
Q

Define: obstetric cholestasis

A

Inactivity of the bile acids from the liver, so bile acids build up in the blood

478
Q

Presentation: obstetric cholestasis

A

Typically presents after 28 weeks
- itching = esp palms of hands and feet
- fatigue
- dark urine
- pale, greasy stools
- jaundice
NO RASH

479
Q

Investigations: Obstetric cholestasis

A

Liver function test and bile acids checked
- abnormal ALT, AST, and GGT
( normal for ALP to increase in pregnancy, placenta produces ALP)
- raised bile acids

rule out other causes:
- gallstones
- acute fatty liver
- autoimmune hepatitis
- viral hepatitis

480
Q

Management: obstetric cholestasis

A
  1. Ursodeoxycholic acid

Itching
- emollients
- antihistamines

  1. Increased risk of stillbirth so planned induction 37-38 weeks
481
Q

What is the testing for fetal Down syndrome?

A
  1. nuchal translucency;
  2. serum testing to measure levels of β-human chorionic
    gonadotropin (β-hCG)
  3. pregnancy-associated plasma protein A (PAPP-A).

can also assess for Edward’s (trisomy 18) and Patau (trisomy 13) syndromes.

482
Q

What is the preconception advice?

A
  • advise regular sex every 2 to 3 days
  • folic acid 0.4 mg
  • aim for BMI 19-30
  • smoking/drinking advice (women no drinking but men within health guidelines)
  • smear
  • rubella
  • aware of environmental/occupational exposure
483
Q

What reproductive disorders are associated with obesity?

A
  • PCOS
  • lower ART success
  • miscarriage
  • infertility
  • obstetric complications
484
Q

Investigations: infertility

A
  1. ovulation/ovarian function/ovarian reserve
    - check mid-luteal progesterone
    (<16 anov, 16-30 equivocal, >30 ovular) = 7 days prior to next period
    - FSH ( day 2)
    - astral follicle count
    - antimullerian hormone
    (<5.4 low response, >25 high response)
    (last 3 mainly for IVF treatment)
  2. semen quality
    - count, motility, morphology, total
    - repeat if abnormal (could be due to illness/ bad day = need 2 abnormal to diagnose semen problem)
    - further test if count <5m/ml (endocrine, karyotype, Cystic fibrosis screen)
    - testicular biopsy = can then freeze sperm

3 tubal patency
- Low risk = hysterosalpingogram (HSG)
- high risk = laparoscopy + dye

485
Q

IVF process

A
  1. ovarian stimulation + monitoring (2 weeks)
  2. egg collection (sedation)
  3. insemination/ICSI
  4. fertilisation check ( day1)
  5. embryo culture (2-5 days)
  6. embryo transfer +/- cryopreservation
  7. luteal support (2 weeks - progesterone)
  8. pregnancy test
486
Q

Management: male infertility

A

Mild
- intrauterine insemination ?
- environment/ lifestyle = occupation, smoking, alcohol, diet, weight

Moderate
- IVF

severe
- IVF with intracytoplasmic sperm injection into the egg

Azoospermia
- surgical sperm removal
- donor insemination

surgery
- correction of epidermal block
- vasectomy reversal
- varicocele - no benefit

Hormonal
- hypogonadotrophic hypogonadism = gonadotrophins
- hyperprolactinaemia = bromocriptin with sexual dysfunction

487
Q

Management: anovulation

A

Group 1 = low FSH/LH/E2
- Give FSH + LH
- GnRH pump
- normalise weight = either too low or high (may need to reduce exercise)

Adenoma = bromocriptine
Sheehan’s = FSH + LH

Group 2 = PCOS
- normal FSH, USS, androgens
- Treatment = ovulation induction e.g. clomifene (or tamoxifen)
(have the eggs just need help releasing them)
- If resistant after 6 cycles = gonadotrophin + then laparoscopic ovarian drilling

Group 3 = premature/menopause
- High FSH
- treatment = donor egg

488
Q

Management: tubal disorders

A
  1. Tubal Surgery (Laparotomy or Laparoscopy)
    Adhesiolysis - 40%
    Salpingostomy - 30%
    Proximal anastamosis - 30%
    Reversal of sterilisation - 60-80%
  2. Tubal catheterisation
    Selective Salpingography - 21%
    Hysteroscopic - 49%
  3. In vitro Fertilisation (IVF) – 30-40%
489
Q

What is the criteria for early infertility referral?

A

Female:
Age > 35
Menstrual disorder
Previous abdominal / pelvic surgery
Previous PID / STD
Abnormal pelvic examination

Male:
Previous genital pathology
Previous urogenital surgery
Previous STD
Systemic Illness
Abnormal genital examination

490
Q

Define + presentation: chorioamnionitis

A

Chorioamnionitis is a clinical diagnosis and is suggested by uterine tenderness and foul-smelling discharge.
- maternal fever,
- tachycardia
- neutrophilia

491
Q

What is a risk factor for chorioamnionitis?

A

Premature rupture of membranes

492
Q

Management: chorioamniotitis

A
  • delivery of baby
  • IV antibiotics
493
Q
A

liquor = the fluid that surrounds baby
Lochia = normal shedding of the decidua discharge/bleeding following delivery
fundus = top of uterus
Decidua = part of the endometrium that allows implantation of blastocyst

494
Q

How does the size of the uterus change after birth?

A
  1. immediately following delivery, uterus contracts fully two level of umbilicus
  2. fundal height then decreases by 1cm/day
  3. returns to pre-pregnancy size at 6 weeks

muscle layer reduces to normal thickness through ischaemia, autolysis and phagocytosis

decidua is shed as lochia

495
Q

What are the types of lochia?

A

LOCHIA RUBRA
Day 0-4
● Blood
● Cervical discharge
● Decidua
● Fetal membrane
● Vernix
● Meconium

LOCHIA SEROSA
Day 4-10
● Cervical mucus
● Exudate
● Fetal membrane
● Micro-organisms
● White blood cells

LOCHIA ALBA
Day 10-28
● Cholesterol
● Epithelial cells
● Fat
● Micro-organisms
● Mucus
● Leukocytes

496
Q

How does prolactin response when breastfeeding?

A

Prolactin response
○ Stimulated through sensation of suckling
○ Hypothalamus disinhibits production of prolactin by
anterior pituitary
○ Through bloodstream to breast to stimulate milk
production

497
Q

How does oxytocin respond in breastfeeding?

A

Oxytocin
○ Stimulated through sensation of suckling as well as
sight/sound/smell of baby
○ Hypothalamus stimulates oxytocin secretion by
posterior pituitary
○ Through bloodstream to stimulate myoepithelial cell contraction leading to milk ejection

498
Q

What is the benefit of breastfeeding for the baby?

A

Improved bonding

Reduced incidence of respiratory and
gastrointestinal disease, otitis media
and necrotising enterocolitis (NEC)

Presence of lactoferrin:
○ Highest in colostrum
○ Improves iron absorption
○ Protects against infections
○ Involved in bone marrow function
○ Boosts immune system functioning

499
Q

What hormones decrease after birth?

A

HCG
Progesterone
oestrogen
Human placental lactogen

500
Q

which hormones increase after delivery?

A

progesterone
oxytocin

501
Q

What is in colostrum?

A

High in protein
Contains IgA and immunoglobulins
higher in glucose

502
Q

What are the red flags of sepsis?

A

RR>25
>2 lactate
systolic bP <90
HR >130
purpuric rash
supplemental O2 requirement
V or less on AVPU

503
Q

What is the sepsis 6?

A

Give 3 and take 3

Give
- fluids
- antibiotics
- oxygen

Take
- blood cultures
- lactate
- fluid balance

504
Q

Presentation: post dural puncture headache

A

Headache worse with sitting/standing
○ Onset 1-7 days post spinal/epidural
○ Neck stiffness
○ Photosensitivity

505
Q

Management: post dural puncture headache

A
  • Lying flat
    ○ Caffeine / fluids
    ○ Simple analgesia
    ○ Epidural blood patch if severe
506
Q

Define: postpartum urinary retention

A

the inability to completely micturate, requiring urinary catheterisation >12h after giving birth OR not to void spontaneously within 6 hours of vaginal delivery

507
Q

What are the causes of postpartum urinary retention?

A
  • Common due to engorgement / trauma to the genital tract following delivery

● Can be related to spinal / epidural anaesthesia

508
Q

define: maternal death

A

death of a patient while pregnant or within 42 days of termination of pregnancy, from any cause related to of aggravated by pregnancy or its management

509
Q

What non-pharmacological pain relief is provided in labour?

A

Water
- may help relaxation

TENS
- gentle electric current passes through pads on their back
- can control strength
- reduces backache in early labour

Alternative therapies
- acupuncture
- acupressure
- hypnotherapy

510
Q

What pharmacological pain relief is offered in labour?

A

Etonox
- nitrous oxide and oxygen
- spaced out, nauseate, tiring, mouth dry
- don’t use when pushing

Diamorphine
- IM/SC injection
- takes about 30 mins to work, lasts a few hours
- casue baby to sleep, slow to breathe
- mother - sickness, sleepiness

PCIA
- remifentanil
- press a button with every contraction
- baby = slow to breathe
- mum = sickness, sleepiness, slow breathing, O2 via nasal cannula

511
Q

Where is the anaesthetic injected into with a epidural and spinal block?

A

Epidural = epidural space

Spinal = subarachnoid space

512
Q

What are the different Caesarean section categories?

A

Cat 1
Delivery within 30 minutes

Cat 2
Delivery within 75 minutes

Cat 3
Delivery within 24 hours

Cat 4
Elective

513
Q
A
514
Q

What are the causes of vaginitis?

A

Non-infectious
- allergic reactions
- normal physiological variation
- atrophic vagintiis
lichen sclerosis

Infectious
- genital herpes
- chlamydia
- gonorrhoea
- trichomonad
- candidia
- bacterial vaginosis

515
Q

What are the risks of IVF?

A

Multiple Pregnancy
Miscarriage
Ectopic
Fetal abnormality?
Ovarian Hyperstimulation Syndrome (OHSS) 1-5% (lower @JW)
Egg Collection (1:2000)
Longer term - ? Ovarian Ca

516
Q

Presentation: vaginitis

A
  • vaginal discharge
  • vulval itching
  • vulval irritation
  • vaginal odour
517
Q

When is IVF offered?

A

Treat after 2 years infertility

women< 40 yrs
- 3 full cycles
- stop once age = 40

women 40-42
- 1 full cycle (if no previous IVF, no low ovarian reserve)
- cancelled cycles don’t count (unless low ovarian reserve)
- private cycles count against total

518
Q

Presentation: bacterial vaginosis

A

MC cause of abnormal discharge
- pH of vaginal fluid increased >4.5
- offensive fishy smelling discharge
- white or grey discharge
- no itching, soreness or irritation

519
Q

What are the risk factors for bacterial vaginosis?

A

Vaginal douching
Receptive cunnilingus
Black race
Recent change of sex partner
Smoking
Presence of an STI e.g. chlamydia or herpes

520
Q

Investigation: bacterial vaginosis

A

gram staining - clue cells
Nugant score

521
Q

Management: bacterial vaginosis

A

Metronidazole 400mg twice daily for 5-7 days
or intravaginal gel

522
Q

Presentation: trichomonas vaginalis

A
  • vaginal discharge = frothy yellow/ green
  • vulval itching
  • dysuria
  • offensive odour
    (+/-) low abdo pain
    (+/-) vulval ulceration.
523
Q

What are the complications of trichomonad vaginalis?

A
  • preterm delivery and low birth weight in pregnancy
  • May predispose to maternal postpartum sepsis
  • May enhance HIV transmission
524
Q

Investigations: trichomonas vaginalis

A
  • swab taken from posterior fornix
  • nucleic acid amplification tests if available
525
Q

Management: trichomonas vaginalis

A

General Advice
Full explanation of diagnosis with written information.
Screening for other STIs

Recommended regimes
Metronidazole 400-500mg twice daily for 5-7 days

Alternative regimens
Tinidazole 2g orally in a single dose

(partners should be treated)

526
Q

Define: vulvovaginal candidiasis

A

acute inflammatory dermatitis of the vulva and vagina
- caused by mucosal invasion of commensal yeast species = Candida albicans

527
Q

Presentation: candida

A

Vulval itch
Vulval soreness
Vaginal discharge = white, cottage cheese
Superficial dyspareunia
External dysuria
excoriation
satellite lesions

528
Q

Investigations: candida

A

vaginal swab from anterior fornix
- gram or wet film examination
- direct plating to solid fungal media

529
Q

Management: un complicated candidiasis

A

general advice:
- Vulval moisturises as soap substitute
- avoid tight fitting synthetic clothing
- avoid irritants

Medical
- Clotrimazole Pessary
- Clotrimazole Vaginal cream (10%)
- Fenticonazole Pessary
- Isoconazole Vaginal tablet
- Miconazole Ovule
- Miconazole Pessary
- Nystatin Vaginal cream
- Nystatin Pessary

530
Q

Management: complicated candidiasis

A

Severe symptoms (a subjective assessment)
Pregnancy
Recurrent vulvovaginal candidiasis (more than 4 attacks per year)
Non-albicans species
Abnormal host (e.g. hyperoestrogenic state, diabetes mellitus, immunosuppression)

treatment
- fluconazole 150mg repeated after 3 days

531
Q

What are the features of mycoplasma genitalium?

A

majority asymptomatic
- urethritis
- urethral disachrge
- dysurai
- penile irritation
- urethral discomfort
- sexually acquired reactive arthritis
- PID
- pre-term delivery
- post-coital bleeding

532
Q

Investigations: mycoplasma genitalium

A

Males
- first void urine

Females
- vulvovaginal swab (viral swab)

test any partners that the patient is planning to have sex with again

533
Q

Treatment: mycoplasma genitalium

A

non-complicated infection
1. doxycycline 100mg BD 7 days followed by azithromycin
2. Moxifloxacin 400mg OD 10 days

Complicated
- moxifloxacin 400mg OD 14 days

534
Q

Define: gonorrhoea

A

Gram negative diplococcus bacteria
- it infects mucous membranes with a columnar epithelium
- spreads via contact with mucous secretions

535
Q

What is the presentation for gonorrhoea?

A

odourless purulent discharge = green or yellow
dysuria
pelvic pain or testicular pain for men

536
Q

Management: Gonorrhoea

A
  1. Nucleic acid amplification testing = detect RNA or DNA present
  2. Single dose of IM ceftriaxone (sensitivities not known)
    Single dose of oral ciprofloxacin (sensitivities KNOWN)
537
Q

What is disseminated goncoccal infection?

A

A complication of untreated gonococcal infection, where the bacteria spreads to the skin and joints.

It causes:

Various non-specific skin lesions
Polyarthralgia (joint aches and pains)
Migratory polyarthritis (arthritis that moves between joints)
Tenosynovitis
Systemic symptoms such as fever and fatigue

538
Q

Define: chlamydia

A

Chlamydia trachomatis = gram negative bacteria causes STI

539
Q

What is the presentation for chlamydia?

A

In women that are sexually active:
Abnormal vaginal discharge
Pelvic pain
Abnormal vaginal bleeding (intermenstrual or postcoital)
Painful sex (dyspareunia)
Painful urination (dysuria)

men that are sexually active and present with:

Urethral discharge or discomfort
Painful urination (dysuria)
Epididymo-orchitis
Reactive arthritis

540
Q

Investigations: chlamydia

A

Nucleic acid amplification tests (NAAT)
- swab checking the DNA/RNA of organism
- swab endocervical, vulvovaginal and then urine

541
Q

Management: chlamydia

A
  1. Doxycycline 100mg twice a day for 7 days
    abstain from sex for 7 days
    inform all partners + refer for testing
    advice on future prevention
542
Q

What are some consequences of chlamydia?

A

Pelvic inflammatory disease
Chronic pelvic pain
Infertility
Ectopic pregnancy
Epididymo-orchitis
Conjunctivitis
Lymphogranuloma venereum
Reactive arthritis

543
Q

What is SARA?

A

Sexually acquired reactive arthritis
- seronegative spondyloarthropathies
- sterile inflammation of the synovial membranes, fascia, and tendons triggered by an infection at a distal site

Causes:
chlamydia
gonorrhoea
mycoplasma genitalium

544
Q

Define = causes: syphillis

A

STI caused by Treponema palladium
- sex
- vertical transmission
- IV drugs
- blood transfusion

545
Q

Presentation: syphilis

A

Primary
- painless genital ulcer = chancre
- local lymphadenopathy

Secondary
- maculopapular rash
- wart lesions
- fever
- alopecia
- oral lesions

Tertiary
- gummatous lesions
- aortic aneurysms
- neurosyphilis

Neurosyphilis
- headache
- altered behaviour
- dementia
- paralysis

546
Q

Management: syphilis

A

Antibody testing = PCR or dark field microscopy

IM benzathine benzylpenicillin

547
Q
A