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Phase 3a > Obs & Gynae > Flashcards

Obs & Gynae Flashcards

1
Q

↑↑Define screening

A

Screening is the process of identifying apparently healthy people who may have an increased chance of a disease or condition

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2
Q

What is the UK national screening committee criteria?

A

The condition: should be an important health problem judged by severity and/or frequency
The test: should be simple, safe, precise and validated screening test which is acceptable to the target population and an agreed policy on further diagnostic investigation for positive results
The intervention: effective intervention with evidence of better outcomes for the individual compared to usual care with wider benefits relating to family members
the screening programmes: evidence from RCTs that programme js effective in reducing morbidity and mortality
implementation criteria: including quality standards, adequate trained staff & facilities, evidence based patient information

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3
Q

List the antenatal screening programmes

A

Sickle cell and Thalassemia
Infectious diseases screening
Down’s Edwards’ and Patau’s syndrome screening
Fetal anomaly scan
Diabetic eye screening

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4
Q

List the newborn screening programmes

A

Newborn infant physical examination
Newborn hearing screen
Newborn blood spot

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5
Q

6 points

What are the components of the screening pathway?

A

Identify the eligible population
Provide information
Explain the conditions, purpose of screening, the test, limitations, results pathways, treatment options
Document the decision to accept/decline
Perform the test
Communicate the results and document in notes/maternity system
Ensure timely transition into appropriate follow-up and treatment for those that screen positive
Optimise health outcomes

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6
Q

What are the 2 types of haemoglobinopathies?

A
  1. unusual genes that affect quality and structure of Hb
  2. unusual genes that affect the quantity of Hb
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7
Q

When should babies born to mothers with Heb B be vaccinated?

A

24 hours of birth and at 4,8,12 and 16 weeks & 12 months

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8
Q

Which infectious diseases are part of the screening for pregnant women?

A

Syphilis, HIV, Hep B

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9
Q

Which infectious diseases are part of the screening for pregnant women?

A

Syphilis, HIV, Hep B

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10
Q

When is combined testing recommended for Down’s, Edwards and Patau’s?

A

11 weeks + 2 days to 14 weeks and 1 day

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11
Q

Describe Patau’s syndrome

A

Trisomy 13
Incidence increases with maternal age
Most babies with T13 will die before they are born, be stillborn or die shortly after birth → 80% have congenital heart defects, holoprosecephaly, midline facial defects, abdominal wall defects, urogenital malformations, abnormalities of hands and feets

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12
Q

What are gonadotrophins?

A

The hormones produced to control the reproductive system

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13
Q

Which hormones are involved in the HPG axis?

A

gonadotrophin releasing hormone (GnRH), luteinising hormone (LH) and follicle stimulating hormone

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14
Q

Where are each of the hormones released from in the HPG axis?

A

hypothalamus: GnRH
anterior pituitary: LH and FSH

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15
Q

Describe how the female gonadal axis works?

A
  1. hypothalamus secretes GnRH
  2. GnRH travels to the anterior pituitary and binds to the receptors on the gland
  3. LH and FSH released
  4. Bind to the ovaries to stimulate production of oestrogen and inhibin
  5. incresing levels of oestrogen and inhibi have a -tive feedback on the pituitary and hypothalamus
  6. this leads to ↓ production of GnRH, LH & FSH
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16
Q

How do LH and FSH work on the ovaries?

A

They stimulate the follicles in the ovaries. The theca granulosa cells around the follicles secrete oestrogen. Oestrogen has a negative feedback on the hypothalamus/anterior pituitary

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17
Q

What type of hormone is oestrogen?

A

steroid sex hormone

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18
Q

What type of hormone is oestrogen?

A

steroid sex hormone

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19
Q

What does oestrogen do?

A

Acts on oestrogen receptors to stimulate:
* breast tissue development
* growth and development of sex organs
* blood vessel development of the uterus
* development of the endometrium

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20
Q

What does oestrogen do?

A

Acts on oestrogen receptors to stimulate:
* breast tissue development
* growth and development of sex organs
* blood vessel development of the uterus
* development of the endometrium

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21
Q

What type of hormone is progesterone?

A

steroid sex hormone

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22
Q

What type of hormone is progesterone?

A

steroid sex hormone

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23
Q

When and where is progesterone produced?

not in pregnancy

A

produced by the corpus luteum after ovulation

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24
Q

When and where is progesterone produced?

in pregnancy

A

Produced by the placenta from 10 weeks gestation onwards

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25
Q

What does progesterone do?

A

Thicken and maintain the endometrium
Thicken the cervical mucus
Increase the body temperature

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26
Q

What are the 2 phases of the menstrual cycle?

A

Follicular phase and luteal phase

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27
Q

How long does each phase of the menstrual cycle last?

A

Follicular: from start of menstruation to moment of ovulation (first 14 days in a 28 day cycle)

Luteal: from moment of ovulation to the start of menstruation (the final 14 days of the cycle)

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28
Q

What are follicles?

A

Granulosa cells surround the oocytes, forming the follicles

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29
Q

What are the 4 stages of development of a follicle?

A
  1. primordial follicles
  2. primary follicles
  3. secondary follicles
  4. antral follicles (graafian follicles)
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30
Q

Describe stages 1, 2 & 3 of the development of a follicle?

A

Primordial follicles → primary & secondary follicles always occurs independent of the menstrual cycle. Once the follicles reach the secondary follicle stage, they develop the receptors FSH.

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31
Q

What happens to the follicles during the follicular stage of the menstrual cycle?

A

At the start of the menstrual cycle, FSH stimulates further development of the secondary follicles.
As the follicles grow, the granulosa cells that surround them secrete increasing amounts of oestradiol (oestrogen)
The oestrogen has a -tive feedback on the HPG
The rising oestrogen also causes the cervical mucus to become more permeable, allowing sperm to penetrate the cervix around the time of ovulation.
One of the follicles will develop further than the others and become the dominant follicle.

LH spikes just before ovulation causing the dominant follicle to release the ovum from the ovary.

Ovulation happens 14 days before the end of the cycle

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32
Q

Describe the luteal phase?

A

After ovulation, the follicle that released the ovum collapses and becomes the corpus luteum.
The corpus luteum

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33
Q

What are the two stages of the first stage of labour called?

A

Latent
Active

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34
Q

Describe the latent and active stages?

A

Latent: time taken for cervix to fully efface and dilate up to 3cm

Active: time taken from 3cm to the cervix being fully dilated

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35
Q

How does cervical ripening occur?

A

Oestrogen, relaxin and prostaglandins break down the cervical connective tissues → which involves a reduction in collagen, an increase in glycosaminoglycans, reduced aggregation of collagen fibres and an increase in hyaluronic acid

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36
Q

How are prostaglandins produced in the third trimester?

A

By the placenta, the uterine decidua, the myometrium and the membranes

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37
Q

Describe primary PPH

A

bleeding within 24 hours of birth

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38
Q

Describe secondary PPH

A

From 24 hours to 12 weeks after birth

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39
Q

What are the causes of primary PPH?

A

T- tone (uterine atony)
T- Trauma (eg perineal tear)
T- tissue (retained placenta)
T- thrombin (bleeding disorders)

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40
Q

What are the risk factors for PPH?

A

previous PPH
multiple pregnancy
obesity
large baby
failure to progress in the second stage of labour
pre-eclampsia
placenta accreta
retained placenta
instrumental delivery
general anaesthesia
episiotomy or perineal

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41
Q

What are the preventative measures for PPH?

A

Treating anaemia during the antenatal period
Giving birth with an empty bladder (full bladder reduces uterine contractions)
Active management of the third stage (IM oxytocin)
IV TXA can be used during c section for high risk patients

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42
Q

What is the management for PPH?

A

Obstetric emergency and needs to be managed by an experienced team including senior midwives, obstetricians, anaesthetics

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43
Q

What are the mechanical treatments for PPH?

A

Rubbing the uterus through the abdomen stimulates uterine contractions
Catheterisation (bladder distention prevents uterus contractions)

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44
Q

Describe the bacteria that causes syphilis

A

It is caused by treponema pallidum. It is spirochete and gets in through skin or mucous membranes where it replicates and then disseminates. The incubation period is 21 days

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45
Q

How is syphilis transmitted?

A

Oral, vaginal or anal sex through direct contact with the infected area

vertical transmission from mother to baby during pregnancy

IV drug use

Blood transfusions and other transplants

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46
Q

Describe the stages of syphilis

A

Primary: painless ulcer called a chancre at the site of the original infection

Secondary: systemic symptoms including the skin and mucous membranes. These symptoms can resolve after 3-12 weeks and the patient can enter the latent stage

latent stage: occurs after secondary stage where symptoms disappear. Early latent occurs within 2 years of initial infection and late latent syphilis occurs from 2 years onwards

tertiary syphilis: can occur many years after the initial infection and affect many organs of the body, particularly with the development of gummas and cardiovascular/neuro symptoms

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47
Q

What are the symptoms of primary syphilis?

A

painless genital ulcer (chancre)
local lymphadenopathy

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48
Q

What are the symptoms of secondary syphilis?

A

maculopapular rash
condylomata lata (grey wart lesions around the genitals or anus)
low grade fever
lymphadenopathy
alopecia
oral lesions

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49
Q

what are the symptoms of tertiary syphilis?

A

gummatous lesions → gummas are granulomatous lesions that can affect the skin, organs and bones

aortic aneurysms

neurosyphilis

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50
Q

what are the symptoms of neurosyphilis?

A

can occur at any stage if infection reaches CNS

headache
altered behaviour
dementia
tabes dorsalis (demyelination affecting the spinal cord posterior columns
ocular syphilis
paralysis
sensory impairment

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51
Q

What is the argyll robertson pupil?

A

A specific finding in neurosyphilis

It is a constricted pupil that accomodates when focusing on a near object but does not react to light

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52
Q

What are the investigations for syphilis?

A

dark ground microscopy of chancre fluid detects spirochete in primary syphilis

PCR testing of swab from active lesion

Serology:

-treponemal tests assesses for exposure to treponemes eg treponemal IgG/IgM

Non-treponemal tests:

  • RPR/VDRL: rises in early disease, falling titres indicate successful treatment or progression to late disease

lumbar puncture: CSF antibody tests in neurosyphilis

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53
Q

What is the management of syphilis?

A

early syphilis: benzathine penicillin 2.4 MU IM single dose

late syphilis: benzathine penicillin 2.4 MU IM single dose

neurosyphilis: procaine penicillin 1.8 MU - 2.4 MU IM OD plus probenecid 500mg PO QDS for 14 days

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54
Q

Describe the bacteria that causes chlamydia

A

chlamydia trachomatis is a gram negative bacteria that replicates intracelullarly

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55
Q

What are the risk factors for chlamydia?

A

age <25
sexual partner positive for chlamydia
recent change in sexual partner
co-infection with another STI
non-barrier contraception or lack of consistent use of barrier contraception

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56
Q

What are the different serotypes of chlamydia?

A

serotypes A-C cause ocular infection

serotypes D-K responsible for classical genitourinary infection

serotypes L1-L3 cause lympogranuloma venereum, which causes an infection MSM often resulting in proctitis

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57
Q

Describe fibroids

A

Benign tumours of the smooth muscle → uterine leiomyomas. More common in women of later reproductive years & more common in black women. They are oestrogen sensitive

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58
Q

Describe the different types of fibroids

A

Intramural: within the myometrium → distort and change shape of the uterus

Subserosal: just below the outer layer of the uterus. These fibroids frow outwards and can become very large

Submucosal: just below the endometrium

Pedunculated: means on a stalk growing away from the uterus

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59
Q

What are the signs and symptoms of fibroids?

A

Heavy menstrual bleeding
Prolonged menstruation
Abdominal pain worse during menstruation
Bloating or feeling full in the abdomen
Urinary or bowel symptoms due to pelvic pressure or fullness
Deep dyspareunia
Reduced fertility

Abdo/bimanual examination may reveal a palpable pelvic mass or an enlarged firm non-tender uterus

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60
Q

Investigations for fibroids?

A

Hysteroscopy: initial investigation for submucosal fibroids presenting with heavy menstrual bleeding

Pelvic USS: investigation of choice for larger fibroids

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61
Q

Management of fibroids?

A

<3cm fibroids:
medical mx: mirena coil, symptomatic mx w/ NSAIDs and TXA
COCP
oral progestogens
surgical mx: endometrial ablation, resection of submucosal fibroids during hysteroscopy, hysterectomy

> 3cm fibroids:
medical mx: as above
surgical mx: uterine artery embolisation, myomectomy, hysterectomy

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62
Q

How are GnRH agonists used as a management for fibroids?

A

May reduce the size of fibroids before surgery
Induce a menopause-like state and reducing the amount of oestrogen maintaining the fibroid

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63
Q

Define PCOS

A

A common condition causing metabolic and reproductive problems in women
characteristic features: multiple ovarian cysts, infertility, oligomenorrhoea, hyperandrogenism, and insulin resistance

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64
Q

Describe the Rotterdam criteria

A

A diagnosis requires at least 2 of the 3 following key features:

hyperandrogenism characterised by hirsutism and acne
-polycystic ovaries on USS

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65
Q

Presentation of PCOS?

A

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

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66
Q

Other features and complications of PCOS?

A

Insulin resistance & diabetes
Acanthosis nigricans
Cardiovascular disease
Hypercholesterolaemia
Endometrial hyperplasia & cancer
Obstructive sleep apnoea
Depression & anxiety
Sexual problems

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67
Q

Describe the link between insulin resistance and PCOS

A

Pancreas producing more insulin to get a response from the cells of the body
Insulin promotes the release of androgens from the ovaries and adrenal glands
Higher levels of insulin result in higher levels of androgens (eg testosterone)

Insulin also suppresses sex hormone binding globulin production by the liver → SHBG normally binds to androgens and suppresses their function

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68
Q

Investigations for PCOS

A

Blood tests:
Testosterone (↑)
Sex hormone binding globulin
Luteinizing hormone (↑)
Follicle stimulating hormone
Prolactin
Thyroid stimulating hormone

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69
Q

What are the imaging investigations for PCOS?

A

TAUSS is required when suspecting PCOS

TVUSS is the gold standard for visualising the ovaries → the follicles may be arranged around the periphery of the ovary giving a “string of pearls” appearance
Diagnostic criteria: 12 or more developing follicles in one ovary & ovarian volume of more than 10cm3

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70
Q

Management of PCOS?

A

General Mx: weight loss, low glycaemic, exercise, smoking cessation, anti-hypertensive, statins where indicated

Patients should be assessed & managed for associated features & complications →
endometrial hyperplasia & cancer, infertility, hirsutism, acne, obstructive sleep apnoea, depression & anxiety

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71
Q

Define endometrial cancer?

A

Cancer of the endometrium, an oestrogen dependent cancer, most cases are adenocarcinomas

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72
Q

RF for endometrial cancer?

A

Anything that increases the patient’s exposure to unopposed oestrogen (oestrogen without progesterone)

-older age
-earlier onset of menstruation
-late menopause
-oestrogen only hormone replacement therapy
-no or fewer pregnancies
-obesity
-PCOS
-tamoxifen

plus T2DM

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73
Q

Why is PCOS a risk factor for endometrial cancer?

A

Due to lack of ovulation: no corpus luteum is produced so less progesterone is produced and so this increased the exposure of the endometrial lining to unopposed oestrogen

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74
Q

Why does obesity increase risk of endometrial cancer?

A

Adipose is a source of oestrogen in post menopausal women. Adipose tissue contains aromatase which converts androgens into oestrogen

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75
Q

Protective factors against endometrial cancer?

A

COCP
Mirena coil
Increased pregnancies
Smoking

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76
Q

Why is smoking a protective factor in endometrial cancer?

A

It is protective in post menopausal women by being anti-oestrogenic.

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77
Q

Presentation of endometrial cancer?

A

Postmenopausal bleeding (ALWAYS A RED FLAG!!)
Intermenstrual bleeding
Unusually heavy menstrual bleeding
Abnormal vaginal discharge
Haematuria
Anaemia
Raised platelet count

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78
Q

Investigations for endometrial cancer?

A

TVA for endometrial thickness (should be <4mm post menopause)
Pipelle biopsy
Hysteroscopy for endometrial biopsy

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79
Q

Stages of endometrial cancer?

A

Stage I: confined to the uterus
Stage II: Invades the cervix
Stage III: invades the ovaries, fallopian tubes, vagina or lymph nodes
Stage IV: invades bladder, rectum or beyond the pelvis

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80
Q

Management of endometrial cancer?

A

Stage I & II: total hysterectomy with bilateral salpingo-oophorectomy

Radiotherapy
Chemotherapy
Progesterone

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81
Q

Define cervical cancer?

A

Tends to affect younger women, peaking in the reproductive years. Most common type is squamous cell carcinoma followed by adenocarcinoma. Strong associations with HPV

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82
Q

Which types of HPV are associated with cervical cancer?

A

Types 16 & 18
Types 6 & 11 cause genital warts

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83
Q

How does HPV promote the development of cancer?

A

P53 and pRb are tumour suppressor genes. HPV produces 2 proteins (E6 & E7). E6 inhibits P53 and E7 inhibits pRb.

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84
Q

Risk factors for cervical cancer?

A

Increased risk of catching HPV
Later detection of precancerous and cancerous changes (non-engagement with screening)
Smoking
HIV
COCP used for more than 5 years
Increased number of full term pregnancies
Family hx
Exposure to diethylstilbestrol during foetal development

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85
Q

Presenting symptoms of cervical cancer?

A

Abnormal vaginal bleeding
Vaginal discharge
Pelvic pain
Dyspareunia

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86
Q

Describe cervical cancer screening

A

Smear performed during a speculum examination. Cells collected are transported by liquid based cytology

The samples are initially tested for high risk HPV → if the sample is HPV negative then the smear is considered negative and the cells are not examined.

Women attend every 3 years aged 25-49 and then every 5 years aged 50-64

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87
Q

Which women are screened more regularly for cervical cancer?

A

Women with HIV are screened annually
Women over 65 may request a smear if they have not had one since aged 50
Women with CIN may require additional tests
Groups of immunocompromised women may have additional screening eg women on dialysis, cytotoxic drugs or undergoing an organ transplant
Pregnant women due a routine smear should wait until 12 weeks post partum

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88
Q

What are the cytology results after a smear?

A

Inadequate
Normal
Borderline changes
Low grade dyskaryosis
High grade dyskaryosis (moderate )
High grade dyskaryosis (severe)
Possible invasive squamous cell carcinoma
Possible glandular neoplasia

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89
Q

Management of smear results?

A

Inadequate sample: repeat in 3 months
HPV -tive: continue with routine screening
HPV +tive w/ normal cytology: repeat the HPV test after 12 months
HPV +tive with abnormal cytology: refer for colposcopy

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90
Q

Describe colposcopy?

A

Colposcope is used to magnify the cervix. Acetic acid causes abnormal cells to appear white → occurs in cells with more nuclear material eg cervical intraepithelial neoplasia and cervical cancer cells
Schiller’s iodine test: uses iodine solution to stain the cells of the cervix. Iodine will stain the healthy cells a brown colour. Abnormal areas will not stain. A punch biopsy or large loop excision of the transformational zone can be performed during the colposcopy procedure.

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91
Q

Mx of cervical cancer?

A

CIN or early stage 1a: LLETZ or cone biopsy
1B-2A: radical hysterectomy and removal of local lymph nodes with chemotherapy and radiotherapy
2B-4A: chemo- & radiotherapy
4A: a combination of surgery, radiotherapy, chemotherapy and palliative care

5 year survival drops from 98% at stage 1A to 15% with stage 4

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92
Q

Describe the use of bevacizumab as a treatment of cervical cancer

A

Monoclonal antibody that may be used in combination with other chemotherapies in the treatment of metastatic or recurrent cervical cancer. Targets vascular endothelial growth factor A and so reduces the development of new blood vessels.

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93
Q

Describe the different types of ovarian cancer

A

Epithelial cell tumours: most common subtypes include → serous tumours (most common), endometrioid carcinomas, clear cell tumours, mucinous tumours, undifferentiated tumours

Dermoid cysts/germ cell tumours: benign ovarian tumours, they are teratomas. Associated with ovarian torsion. May cause raised alpha fetoprotein and hCG

Sex cord stromal tumours: rare tumours, can be benign or malignant. Arise from the stroma or sex cords.

Krukenberg tumour: metastasis in the ovary usually from a GI tract cancer

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94
Q

Risk factors for ovarian cancer?

A

Age (peaks @ 60)
BRCA1 & BRCA2 genes
Increased number of ovulations (early menarche, late menopause, no pregnancies)
Obesity
Smoking
Recurrent use of clomifene

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95
Q

Protective factors for ovarian cancer?

A

Factors that stop ovulation or reduce the number of life time ovulations

COCP
Breast feeding
Pregnancy

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96
Q

Presentation of ovarian cancer?

A

Abdo bloating
Early satiety
Loss of appetite
Pelvic pain
Urinary symptoms
Weight loss
Abdo or pelvic masses
Ascites
Referred groin or hip pain due to mass pressing on the obturator nerve

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97
Q

Investigations for ovarian cancer?

A

CA 125 (cancer antigen) blood test : >35
Pelvic USS
CT scan to establish diagnosis and stage the cancer
Histology
Paracentesis

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98
Q

Other causes of raised CA125?

A

Endometriosis
Fibroids
Adenomyosis
Pelvic infection
Liver disease
Pregnancy

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99
Q

MoA of the COCP?

A

Prevents ovulation → oestrogen & progesterone have a -tive feedback on the hypothalamus & pituitary so suppress the release of GnRH, LH & FSH so ovulation does not occur

Progesterone thickens the cervical mucus

Progesterone inhibits proliferation of the endometrium, reducing the chance of successful implantation

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100
Q

Types of COCP?

A

Monophasic pills: contain the same amount of hormone in each pill
Multiphasic pills: contain varying amounts of hormone to match the normal cyclical hormonal changes more closely

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101
Q

S/E & risks of COCP?

A

Breast pain and tenderness
Mood changes and depression
Headaches
Hypertension
VTE
Small increased risk of breast & cervical cancer returning to normal 10 years after stopping
Small increased risk of MI and stroke

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102
Q

Benefits of COCP

A

Effective contraception
Rapid return of fertility after stopping
Improvement in PMS, menorrhagia & dysmenorrhoea
Reduced risk of endometrial, ovarian & colon cancer
Reduced risk of benign ovarian cysts

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103
Q

Contraindications of the COCP?

A

Uncontrolled HTN
Migraine with aura
Hx of VTE
>35 & smoking >15 cigarettes a day
Major surgery with prolonged immobility
Vascular disease or stroke
Ischaemic heart disease, cardiomyopathy or AF
Liver cirrhosis and liver tumours
SLE & antiphospholipid syndrome
BMI >35

104
Q

When can the COCP be started?

A

Starting on the first day of the period offers protection straight away and for up to day 5, no additional protection is needed
Starting after day 5 needs additional protection for the first 7 days of consistent pill use
When switching between COCPs, finish one pack and immediately start the next without a break in the middle

105
Q

Missed pill rules for COCP?

A

Miss one pill: take the missed pill as soon as possible, no extra protection required if the other pills before and after are taken correctly

Missing more than one pill:
Take the most recent missed pill as soon as possible and use additional contraception until they have taken the pill for 7 days straight

If on days 1-7: need emergency contraception if have had unprotected sex (bc have just had a pill free break and must have taken it for 7 days beforehand for it to be effective)

If on days 8-14: no emergency contraception is required if they were fully compliant on days 1-7

If on days 15-21: if days 1-14 were fully compliant then no emergency contraception needed but should go back to back with their next packet and not skip the pill free period

106
Q

What can reduce the effectiveness of the pill?

A

V&D (a day of this is classed as a missed pill day)
Rifampicin

107
Q

What is the progestogen only pill?

A

Contains only progesterone and is taken continuously. It has few risks and contraindications than the COCP

108
Q

Types of PoP?

A

Traditional: cannot be delayed by more than 3 hours
Desogestrel only pill: can be taken up to 12 hours late and still be effective

109
Q

MoA of traditional PoP?

A

Thickening the cervical mucus
Altering the endometrium and making it less accepting of implantation
Reducing the ciliary action in the fallopian tubes

110
Q

MoA of desogestrel pill?

A

Inhibits ovulation
Thickens the cervical mucus
Alters the endometrium
Reduces the ciliary action of the fallopian tubes

111
Q

When can the PoP be started?

A

Starting on day 1-5 of the cycle means the woman is protected immediately

If started at other times of the cycle, additional contraception is required for only 48 hours bc it takes only 48 hours for the cervical mucus to thicken enough to prevent the sperm entering the uterus

112
Q

Rules for switching from COCP to a PoP?

A

Can start the PoP immediately without additional contraception if they have taken the COCP consistently for more than 7 days ie in week 2 or 3 of the pill pack or re on days 1-2 of the hormone free period following a full pack of the COCP

If they have not had unprotected sex since day 3 of the hormone free period, they can start the PoP immediately but require additional contraception for the first 48 hours of taking the PoP

If they have had unprotected sex since day 3 of the hormone free period they should take the COCP for 7 days consecutively

113
Q

Define endometriosis

A

A condition where there is ectopic endometrial tissue outside the uterus. This is called an endometrioma. Endometriomas in the ovaries are often called chocolate cysts.

114
Q

Define adenomyosis

A

Endometrial tissue within the myometrium

115
Q

Causes of endometriosis?

A

Retrograde menstruation allows endometrial tissue to ‘seed’ the pelvis and abdomen
Embryonic cells destined to become endometrial tissue may remain in areas outside the uterus during the development of the foetus
May be spread of endometrial tissue via the lymphatic system similar to cancer
Cells outside the uterus undergo metaplasia and become endometrial cells

116
Q

Pathophysiology of endometriosis?

A

The cells of the endometrial tissue outside the uterus respond to hormones in the same way endometrial tissues responds to hormones inside the uterus.
The irritation and inflammation of this endometrial tissue outside the uterus leads to cyclical, dull, heavy or burning pain that occurs during menstruation

Deposits of endometriosis in the bladder or bowel can lead to blood in the stool or urine

Localised bleeding & inflammation can lead to adhesions eg fixing the ovaries to the peritoneum

117
Q

Presentation of endometriosis?

A

Cyclical abdominal or pelvic pain
Deep dyspareunia
Dysmenorrhoea
Infertility
Cyclical bleeding from other sites eg haematuria
Cyclical bowel or bladder symptoms

O/E: endometrial tissue visible in the vagina on speculum examination
A fixed cervix on bimanual examination
Tenderness in the vagina, cervix and adnexa

118
Q

Investigations for endometriosis?

A

Pelvic USS: can reveal large endometriomas and chocolate cysts. Can also be unremarkable

Laparoscopic surgery: gold standard to diagnose abdominal and pelvic endometriosis. A definitive diagnosis can be made with a biopsy of the lesions during the laparoscopy.

119
Q

Mx of endometriosis?

A

Hormonal mx: COCP/ PoP/ Mirena coil/ GnRH agonists

Surgical mx: laparoscopic surgery to excise or ablate the endometrial tissue/ hysterectomy

120
Q

Presentation of adenomyosis?

A

Painful periods, heavy periods, dyspareunia, can also present with infertility or pregnancy related complications

121
Q

Investigations for adenomyosis?

A

TVUSS: first line investigation for suspected adenomyosis

Histological examination of the uterus after a hysterectomy

122
Q

Mx of adenomyosis?

A

TXA- reduces bleeding
Mefenamic acid- reduces bleeding and pain as is an NSAID

Contraceptive Mx:
Mirena coil
COCP
Cyclical oral progestogens

123
Q

Pregnancy complications related to adenomyosis?

A

Infertility
Miscarriage
Preterm birth
Small for gestational age
Preterm premature rupture of membranes
Malpresentation
Need for C section
PPH

124
Q

What are ovarian cysts?

A

Cysts are fluid filled sacs. Functional ovarian cysts related to the fluctuating hormones of the menstrual cycle are very common in premenopausal women and are benign.

Cysts in post menopausal women need to be investigated for possible malignancy

125
Q

How do ovarian cysts present?

A

Most ovarian cysts are asymptomatic. Occasionally cause:
Pelvic pain
Bloating
Fullness in the abdomen
A palpable pelvic mass

126
Q

Describe functional cysts?

A

Follicular: represent the developing follicle. When these fail to rupture and release the egg, the cyst can persist. They are harmless and tend to disappear over a few menstrual cycles. Typically have thin walls and no internal structure on USS

Corpus luteum cysts: occur when the corpus luteum fails to break down and instead fills with fluid. They may cause pelvic discomfort, pain or delayed menstruation. Often seen in early pregnancy.

127
Q

Describe the other types of ovarian cysts?

A

Serous cystadenoma: benign tumour of the epithelial cells

Mucinous cystadenoma: benign tumour of the epithelial cells. Can become huge and take up a lot of space in the pelvis and abdomen.

Endometrioma: lumps of endometrial tissue

Dermoid cysts/germ cell tumour:

128
Q

Definition of placenta praevia

A

Low lying placenta: placenta w/in 20mm of the internal os
Placenta praevia: placenta is over the internal os

It is a notable cause of antepartum haemorrhage

129
Q

Risk factors for placenta praevia?

A

Previous c sections
Previous placenta praevia
Older maternal age
Maternal smoking
Structural uterine abnormalities
Assisted reproduction eg IVF

130
Q

Signs and symptoms of placenta praevia?

A

Mostly asymptomatic but may present with painless red vaginal bleeding, soft uterus and high or abnormal foetal lie

131
Q

Investigations for placenta praevia?

A

20 week scan: measure distance of placenta from os and repeat at 32, 34 and 36 weeks based on results.

TVUSS is gold standard

132
Q

Management of placenta praevia?

A

Asymptomatic/identified on scan: watch and wait, avoid bimanual exams, elective c sections recommended from 34 weeks to 36 + 6 to avoid mum going into spontaneous labour

Bleeding: APH protocol, stabilise mum first, speculum exam, steroids for foetus, emergency C section if in labour or unable to stabilise

133
Q

What are the morbid adherent disorders of the placenta?

A

Placenta accreta, increta and percreta.

Where defective decidua basalis leads to the placenta implanting deeper into the endometrium, myometrium and beyond.

Accreta attaches, increta invades and percreta pass through the myometrium

134
Q

Signs and symptoms for accreta, increta or percreta?

A

Usually asymptomatic during the pregnancy. APH in second trimester or difficulty delivering the placenta

135
Q

Investigations for accreta, increta or percreta?

A

20 week USS: loss of definition between wall of uterus and abnormal vasculature

MRI: assess depth and width of invasion

136
Q

Management of accreta, increta and percreta?

A

Identified during scans: elective c section at 36 or 37 weeks, hysterectomy preferred and antenatal steroids.

Identified during elective c section: may close and delay delivery to get specialist team and level 2 HDU bed.

Identified after delivery: hysterectomy recommended.

137
Q

Define placental abruption?

A

Obstetric emergency: placenta detaches from uterine wall during pregnancy.

Revealed: blood loss PV
Concealed: blood loss retained in uterus

138
Q

Risk factors for placental abruption?

A

Trauma
Previous abruption
Pre-eclampsia
Chronic HTN
chorioamnionitis
Uterine malformations
Smoking
Cocaine use

139
Q

Signs and symptoms of placental abruption?

A

Woody/hard/tense uterus, sudden onset severe continuous abdominal pain, APH, maternal shock out of proportion with blood loss, uterine tenderness, continuous lower back pain

140
Q

Investigations of placental abruption?

A

USS: exclude praevia
Kleihauer: assess amount of foetal and maternal blood mixing

141
Q

Management of placental abruption?

A

Small: monitoring, antenatal steroids from 24 weeks to 34 + 6
Large: APH protocol, tranexamic acid, delivery required immediately

142
Q

Risk factors for HTN in pregnancy?

A

older women, obesity, family hx, those who developed HTN when taking the COCP

143
Q

Causes of HTN in pregnancy?

A

Primary/idiopathic

Secondary: obesity, diabetes, renal disease

144
Q

Signs and symptoms of HTN in pregnancy?

A

Few symptoms. Proteinuria may be present in patients with renal disease

145
Q

Management of HTN in pregnancy?

A

Aspirin prophylaxis from 12 weeks onwards due to higher risk of pre-eclampsia

1st line: labetalol
2nd line: nifedipine

Delivery @ 38-40 weeks

146
Q

Define pre-eclampsia?

A

New onset HTN with end organ dysfunction, usually proteinuria (++) after 20 weeks gestation.

147
Q

Pathophysiology of pre-eclampsia?

A

Abnormal invasion of trophoblasts into maternal spiral arteries → leads to high vascular resistance in these vessels

148
Q

Risk factors for pre-eclampsia?

A

HTN in previous pregnancy, CKD, autoimmune disease (SLE, anti-phospholipid), diabetes T1 or T2, chronic HTN, nulliparity, increased maternal age, >10 years between pregnancies

149
Q

Signs and symptoms of pre-eclampsia?

A

Triad: new onset HTN of >140/90 after 20 weeks, proteinuria & oedema

Along with severe headache, hyperreflexia, visual disturbances, papilledema, RUQ pain

150
Q

Investigations for pre-eclampsia?

A

Bloods: abnormal liver enzymes, thrombocytopaenia (monitoring for HELLP syndrome)

Placental growth factor (GOLD STANDARD)

Urine dip +++ proteinuria

151
Q

Management of pre-eclampsia?

A

Stabilise BP: 1st line labetalol 2nd line nifedipine

Admission if BP >160/110

Magnesium sulphate if <34 weeks or neurological signs eg hyperreflexia

Aspirin from 12 weeks for high risk patients

152
Q

Complications of pre-eclampsia?

A

Progression to pre-eclampsia, IUGR, prematurity, maternal organ damage, haemorrhage

153
Q

What is eclampsia?

A

Seizures associated with pre-eclampsia

154
Q

Management of eclampsia?

A

IV magnesium sulphate

155
Q

What is HELLP syndrome?

A

A combination of features that occurs as a complication of pre-eclampsia and eclampsia.

Haemolysis
Elevated Liver enzymes
Low Platelets

156
Q

Define Pelvic Inflammatory Disease (PID)

A

Inflammation and infection of the organs of the pelvis

157
Q

Pathophysiology of PID?

A

Ascending infection of upper genital tract most commonly due to an STI eg chlamydia or gonorrhoea

Other causes include E. Coli, H. Influenzae

158
Q

Risk factors for PID?

A

Young age, multiple sexual partners, not using barrier contraception, STIs, IUD

159
Q

Signs and symptoms of PID?

A

Bilateral lower abdominal pain, deep dyspareunia, abnormal vaginal bleeding, lower abdominal tenderness, mucopurulent cervical discharge, inflammation and infection of the cervix, fever

160
Q

Investigations for PID?

A

Bloods: FBC, CRP, ESR, HIV & syphilis
1st line: High vaginal and endocervical swabs
NAAT for chlamydia, gonorrhoea, mycoplasma, BV, candidiasis & trichomoniasis
Diagnostic lap & biopsy: fimbriae biopsy and culture is gold standard

161
Q

Management of PID?

A

GUM referral, start abx before swabs return

Triple therapy: IM ceftriaxone, then oral doxycycline & metronidazole

OR oral ofloxacin & oral metronidazole

162
Q

Complications of PID?

A

Sepsis, abscess, infertility, chronic pelvic pain, ectopic pregnancy

163
Q

Risk factors for breast cancer?

A

F>M, increasing age, significant fhx eg BRCA 1/2, radiotherapy <35yo, HRT, increased alcohol consumption

164
Q

Screening for breast cancer?

A

Women 50-70yo every 3 years
MRI in <40yo in high risk patients

165
Q

Signs and symptoms of breast cancer?

A

Asx: picked up on screening

Lump in breast, thickened skin/swelling of breast or axilla, orange peel appearance to skin, discharge to nipple/changes to nipples, tugging/indenting of skin

166
Q

Mx of breast cancer?

A

Surgery: wide local excision/mastectomy +/- lymph nodes

Chemo:
ER+ve: tamoxifen for young women and anastrozole for older women
HER+ve: herceptin (younger women) and trastuzumab

167
Q

Define hyperemesis

A

severe form of nausea and vomiting in pregnancy

168
Q

Pathophysiology of hyperemesis?

A

Beta HCG is thought to be the cause so higher levels may mean more severe nausea and vomiting

169
Q

Risk factors for hyperemesis?

A

Multiple or molar pregnancies, nulliparity, increased BMI, hypothyroidism

170
Q

Protective factors for hyperemesis?

A

Smoking

171
Q

Criteria for admission for hyperemesis?

A

weight loss <5%, dehydration, severe nausea and vomiting, electrolyte imbalance, urinary ketones ++

172
Q

Management of hyperemesis?

A

Rest, avoid triggers, ginger, acupressure

Antiemetics: chlorpromazine or 2nd line (antihistamines) ondansetron/metochlopramide

Rehydration in hospital with normal IV fluids and potassium replacement

173
Q

Complications of hyperemesis?

A

Wernicke’s encephalopathy, mallory-weiss tear, AKI, small risk of SGA or pre term birth

174
Q

Pathophysiology of GDM?

A

Pregnancy is a state of physiological insulin resistance and relative glucose intolerance
- fasting levels are ↓
- serum levels post meal are increased vs pre-pregnancy levels

In second and third trimester insulin resistance ↑

175
Q

RF for GDM?

A

Previous GDM, previous macrosomic babies (>4.5kg), BMI >30, Fhx of first degree relative, black, carribbean, african or south asian ethnicity

176
Q

Risks of GDM?

A

Foetal macrosomia (estimated birth weight >4kg)
Shoulder dystocia
Perinatal mortality
Neonatal hypoglycaemia

Greater risk of developing T2DM within 10-15 years

177
Q

Investigations for GDM?

A

Any women with the risk factors should be screened at 24-28 weeks gestation using OGTT

Women with previous GDM have an early OGTT at 13-14 weeks

Normal results: fasting- <5.6 , 2 houra after the drink <7.8

178
Q

Management for GDM?

A

4 weekly monitoring via USS to monitor foetal growth and amniotic fluid from 28-36 weeks

1st Dietary/education/lifestyle advice
2nd Metformin- acts on the liver decreases intestinal absorption of glucose
3rd Insulin- if metformin doesn’t work or contraindicated

Delivery:
uncomplicated by 40+6
complicated by 37-38+6

179
Q

How is GDM managed postnatally?

A

Stop medication, healthy lifestyle advice, contraception

HbA1c @ 13 weeks with GP → 39-47mmol/L is high risk of diabetes and >48mmol/L is diagnostic of T2DM

Annual HbA1c

180
Q

Effects of diabetes (T1/T2) on pregnancy?

A

Insulin dose requirement ↑ in 3rd trimester
Women with diabetic nephropathy may have worsening renal function & proteinuria
Risk of progression or development of retinopathy due to increased glucose control
Hypoglycaemia
Diabetic ketoacidosis- risk in hyperemesis/infection/steroid therapy

181
Q

Complications of diabetes (in pregnancy & normally)?

A

Infections- candida, staph etc
Arterial disease- CVD, peripheral vascular disease
Microvascular disease- retinopathy, nephropathy, neuropathy
Reduced life expectancy due to CVD risks

182
Q

Predisposing factors for DKA in pregnancy?

A

Infection, antenatal steroids, infection, poor control/non drug compliance

183
Q

Maternal risks of pre-existing diabetes?

A

Miscarriage
3x chance of developing pre-eclampsia
Infection- urinary, respiratory, endometrial and wound
Increased chance of c section

184
Q

Foetal risks of pre existing diabetes?

A

Congenital abnormalities- neural tube defects (take folic acid), skeletal abnormalities, congenital heart disease

Perinatal & neonatal mortality/morbidity

Intrauterine foetal death

185
Q

Foetal risks of pre-existing diabetes?

A

Foetal macrosomia
Preterm birth
Neonatal hypoglycaemia
Respiratory distress syndrome

186
Q

Obstetric management of pre existing diabetes?

A

Folic acid 5mg daily
Early dating and viability scan
Dating and nuchal translucency
Aspirin 150mg daily from 12 weeks
USS growth scans 28, 32 and 36 weeks

187
Q

What is obstetric cholestasis?

A

Outflow of bile acids is reduced in pregnancy → build of bile in the blood → leading to itching

188
Q

Risk factors for obstetric cholestasis?

A

Happened in previous pregnancy, South Asian

189
Q

Signs and symptoms of obstetric cholestasis?

A

Itching- worse on soles, palms and abdomen, clinical jaundice, no rash, greasy pale stools, dark urine

190
Q

Investigations for obstetric cholestasis?

A

Bloods- conjugated & unconjugated, serum bile acids increased

LFTs may be normal, bilirubin may be raised

191
Q

Management of obstetric cholestasis?

A

Ursodeoxycholic acid, vitamin K supplements if clotting deranged

Sx management- antihistamines for sleep, topical menthol or calamine emollients

192
Q

What is vasa praevia?

A

When the foetal vessels are within the membranes and pass the internal os

193
Q

Risk factors for vasa praevia?

A

low lying placenta, IVF pregnancy, multiple pregnancy

194
Q

Define ovarian torsion

A

Twisting of the supporting ligaments holding the ovaries in place

195
Q

What is adnexal torsion?

A

Ovarian torsion including the fallopian tubes

196
Q

Risk factors for ovarian torsion?

A

Pregnancy
Ovarian mass
Ovarian hyperstiumaltion syndrome
Reproductive age

197
Q

Signs and symptoms of ovarian torsion?

A

Deep colicky abdo pain
Vomiting
Distressed
May have fever
May have adnexal tenderness on examination

198
Q

Investigations for ovarian torsion?

A

USS- whirlpool sign

199
Q

Management for ovarian torsion?

A

Laparoscopy- detorsion or oophrectomy

200
Q

Why is progesterone given with HRT oestrogen for women with a uterus?

A

Prevents exposure to unopposed oestrogen so reduces risk of endometrial hyperplasia or cancer

201
Q

How is HRT chosen?

A

Local or systemic symptoms?
Local- topical creams/ointments
Systemic- systemic tx eg oestrogen & progesterone

Have a uterus?
Yes- needs both progesterone and oestrogen

Period in the last 12 months?
Yes- cyclical HRT
No- continuous

202
Q

Indications for HRT?

A

Replacing hormones in women with ovarian insufficiency
Reducing vasomotor sx eg hot flushes and night sweats
Improving sx eg low libido, low mood, joint pain etc
Reducing risk of osteoporosis in women <60

203
Q

Risks of HRT?

A

Worse in older women/those with a uterus (endometrial cancer)

Breast cancer- more in combined
Endometrial cancer
VTE
Stroke and CVD

204
Q

Contraindications for HRT?

A

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

205
Q

Risk factors for prolapse?

A

Vaginal birth
Multiparity
Chronic cough/straining
Obesity
Heavy lifting
Pelvic surgery
Connective tissue disorders

206
Q

Gonorrhoea cell type?

A

Gram negative diplococcus

207
Q

Signs and symptoms of gonorrhoea?

A

Endocervicitis/urethritis, purulent discharge, itching

208
Q

Investigations for gonorrohoea?

A

NAAT
Microscopy and culture

209
Q

Management for gonorrhoea?

A

1st line, if sensitivity not known- IM ceftriaxone
If sensitivity known- oral ciprofloxacin

210
Q

What is bacterial vaginosis?

A

Not an STI- overgrowth of anaerobic bacteria if vagina becomes too alkali

211
Q

Risk factors for BV?

A

Multiple sexual partners, excessive vaginal discharge, recent abx, smoking, copper coil

212
Q

Signs and symptoms of BV?

A

Fishy smelling water discharge that is grey/white

Itching and pain not normally associated

213
Q

Investigations for BV?

A

Charcoal swab and microscopy for clue cells

Vaginal pH
Speculum exam

214
Q

Management for BV?

A

None if asymptomatic
1st line- metronidazole
2nd line- clarithromycin

215
Q

Risk factors for urinary incontinence?

A

White women, increased age, post-menopausal, pregnancy, pelvic organ prolapse, pelvic floor surgery, high BMI

216
Q

Signs and symptoms of urge incontinence?

A

Sudden urge to go to the toilet with leakage/not making it

217
Q

Signs and symptoms of stress incontinence?

A

Leakage when increasing intrabdominal pressure eg sneezing, coughing or laughing

218
Q

Investigations for incontinence?

A

Urinalysis
3 day bladder diary
Abdo exam and sims speculum
Urodynamics
Post void bladder scan
Cough test

219
Q

Management for urge incontinence?

A

Conservative: bladder retraining, weight loss, pelvic floor physio

Medical:
1st line- oxybutinin, then tolterodine then solifenacin, mirabegron in the elderly

Surgical:
botox or percutaneous sacral nerve stimulation, cystoplasty

220
Q

Management for stress incontinence?

A

Conservative: avoid caffeine, diuretics and overfilling bladder, weight loss and pelvic floor physio

Medical: duloxetine (2nd line to surgery)

Surgical: autologous fascial sling (supports bladder), intramural urethral bulking (reduces diameter of urethra)

221
Q

Critical complication of lichen sclerosus?

A

squamous cell carcinoma of the vulva

222
Q

Management of lichen sclerosus?

A

Topical steroids in a step down regime followed by emollients

223
Q

What is the organism responsible for trichomoniasis?

A

Trichomoniasis vaginalis is a protozoa that is a single celled organism with a flagella

224
Q

Signs and symptoms of a trichomoniasis infection?

A

50% asymptomatic
frothy green yellow fishy smelling discharge, may also have dysuria and dyspareunia

225
Q

Investigations for trichomoniasis infection?

A

Female: speculum exam showing a strawberry cervix, vaginal pH ↑, charcoal swab of low vagina for microscopy

Male: urethral swab/first catch urine

226
Q

Management for trichomoniasis?

A

Metronidazole single dose 2g or 400mg BD

227
Q

Complications of trichomoniasis?

A

Can increase risk of catching HIV, BV, PID, cervical cancer or pregnancy complications

228
Q

What causes herpes?

A

HSV-1 causes cold sores but can cause genital herpes through oral sex

HSV-2 causes genital herpes but can cause lesions in the mouth

229
Q

How is herpes spread?

A

Spread through direct contact, with the affected mucous membrane/viral shedding into mucous membranes

Virus becomes latent in the associated sensory nerve ganglia after infection

230
Q

Signs and symptoms of a herpes infection?

A

May be asymptomatic for a long time after infection

Sx of initial infection normally occur around 2 weeks afterwards and are most severe- flu like sx, blisters/ulcers, neuropathic pain, dysuria, inguinal lymphadenopathy

231
Q

Investigations for herpes?

A

Full sexual hx including those with cold sores

Dx can be made clinically from examination and hx

Viral PCR swab can confirm dx and causative agent

232
Q

Management for herpes?

A

Aciclovir

Pregnancy:
<28 weeks aciclovir and then prophylactic aciclovir from 36 weeks onwards

> 28 weeks aciclovir but c section advised

233
Q

Risk factors for vulval cancer?

A

Advanced age >75
Immunosuppression
HPV infection
Lichen sclerosus

234
Q

Signs and symptoms of vulval cancer?

A

Most often found on labia majora

Vulval lump
Ulceration
Bleeding
Pain
Itching
Lymphadenopathy in groin

235
Q

Risk factors for ectopic pregnancy?

A

Previous ectopic, fallopian tube surgery or PID
Endometriosis, IUD, increased age, <18 at 1st sexual intercourse, smoking, IVF, >35 at time of presentation

236
Q

Signs and symptoms of ectopic pregnancy?

A

Usually presents at 6-8 weeks pregnancy

Missed period, should tip pain (referred pain), lower abdo/pelvic pain that may be specific, signs of shock, cervical excitation, guarding

237
Q

Investigations for ectopic pregnancy?

A

Pregnancy test, TVUSS → empty gestational sac/tubal pregnancy
Beta hCG

238
Q

Criteria for expectant management of ectopic pregnancy?

A

Follow up needs to be possible to check for successful termination
The ectopic needs to be unruptured
Adnexal mass <35mm
No visible heart beat
No significant pain
hCG level <1500 U/L

239
Q

Medical management of ectopic pregnancy?

A

hCG level must be <5000 U/L
Confirmed absence of intrauterine pregnancy on USS

IM methotrexate and must not get pregnant for at least the next 3 months as is highly teratogenic

240
Q

Surgical management of ectopic pregnancy?

A

Anyone that does not meet the medical or expectant management criteria

First line: laparoscopic salpingectomy to remove fallopian tube and ectopic pregnancy

Second line: laparoscopic salpingotomy preserves the fallopian tube in women with fertility concerns

241
Q

Post partum contraception?

A

IUD- 48 hours PP
IUS- 4 weeks PP
PoP- anytime PP, but if started >21 days PP need additional contraception for 2 days but ok if breast feeding
COCP-
Cannot be started <3 weeks PP due VTE risk
Cannot be used <6 weeks PP if breast feeding
>6 weeks- 6 months breast feeding UKMEC 2

242
Q

Define missed miscarriage?

A

foetus is no longer alive but no symptoms

243
Q

Define threatened miscarriage?

A

Bleeding but foetus still alive and cervical os closed

244
Q

Define inevitable miscarriage?

A

Bleeding and cervical os is open

245
Q

Define incomplete miscarriage?

A

Retained products of conception in uterus after miscarriage

246
Q

Define anembryonic miscarriage?

A

Gestational sac is present but contains no embryo

247
Q

Miscarriage management if <6 weeks?

A

Managed expectantly if no pain, complications or risk factors

A repeat UPT is performed after 7-10 days to confirm that the miscarriage is complete

248
Q

Medical management of miscarriage if >6 weeks?

A

Misoprostol (prostaglandin analogue) softens the cervix and stimulates uterine contractions → dose can be oral or vaginal suppository

s/e heavier bleeding, pain, vomiting, diarrhoea

249
Q

Surgical management of miscarriage if >6 weeks?

A

prostaglandins given before surgery

Manual vacuum aspiration- LA and a syringe is used to aspirate contents out of uterus

Electric vacuum aspiration- GA

250
Q

Medical termination of pregnancy <9 weeks?

A
  1. Mifepristone (prevents placenta forming)
  2. Misoprostol taken 1-2 days later to stimulate uterine contractions
251
Q

Surgical termination of pregnancy >9 weeks?

A

cervical priming- mifepristone and misoprostol and osmotic dilators

252
Q

Surgical termination of pregnancy <14 weeks?

A

Dilation and vacuum/suction aspiration

253
Q

Surgical termination of pregnancy 14-24 weeks?

A

Dilation and extraction

254
Q

Definition of fertility?

A

Failure to conceive after a year a year of unprotected intercourse

255
Q

Causes of infertility?

A

Unexplained
Ovulatory
Tubal
Uterine/peritoneal anatomy
Male

Phase 3a (8 decks)

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