Clinical Flashcards

1
Q

what is primary amenorrhoea ?

A

failure to start menstruating. it needs investigation in a 16-year old, or in a 14 year old who has no signs of puberty

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2
Q

what is secondary amenorrhoea?

A

this is when periods stop for >6 months other than due to pregnancy. occurs after periods were previously occuring.

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3
Q

what is oligomenorrhoea?

A

infrequent periods - common at the extremities of reproductive life when regular ovulation often does not occur

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4
Q

what is menorrhagia?

A

excessive menstrual blood loss -

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5
Q

what is dysmenorrhoea?

A

painful periods (+/- nausea or vomiting)

primary dysmenorrhoea - pain without organ pathology - often starting with anovulatory cycles after the menarche

secondary dysmenorrhoea - pain with associated with pathology e.g. adenomyosis, endometriosis, pelvic inflammatory disease

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6
Q

what is intermenstrual bleeding?

A

vaginal bleeding (other than postcoital) at any time may follow after a mid-cycle fall in oestrogen production

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7
Q

what is postcoital bleeding?

A

non-menstrual bleeding that occurs immediately after sexual intercourse

causes: cervical trauma, polyps; cervical, endometrial and vaginal carcinoma and vaginitis

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8
Q

what is postmenopausal bleeding?

A

bleeding occuring >1yr after the last period.

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9
Q

what is the main cause of postmenopausal bleeding?

A

endometrial carcinoma - always this unless proven otherwise

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10
Q

what are the causes of inter menstrual bleeding?

A

pregnancy related

hormonal contraception

infection: chlamydia and PID

cervical ectropian, polyps and carcinoma

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11
Q

what are other causes of postmenopausal bleeding?

A

oestrogen withdrawal

atrophic vaginitis

cervical polyps

cervical malignancy

endometrial polyps

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12
Q

what are the causes of primary amenorrhoea?

A

1.Physiological causes:

Constitutional delay — no anatomical abnormality

Pregnancy

2.Genito-urinary malformations:

Imperforate hymen - cyclical pain

Transverse septum.

Absent vagina or uterus.

3.Endocrine disorders:

Hypothyroidism.
Hyperthyroidism.
Hyperprolactinaemia

Cushing’s syndrome.

Polycystic ovary syndrome (a rare cause of primary amenorrhoea).

Androgen insensitivity syndrome (rare, previously known as ‘testicular feminization’).

4.Causes of primary amenorrhoea in those with no secondary sexual characteristics (such as breast development) include:
Primary ovarian insufficiency (POI) due to:

Chromosomal irregularities (for example Turner’s syndrome [46XO] and gonadal agenesis [46XX or 46XY]).

5.Hypothalamic dysfunction due to:
Stress, excessive exercise, and/or weight loss

  1. Chronic systemic illness (such as uncontrolled diabetes, severe renal and cardiac disorders, coeliac disease, cancer, and infections [for example tuberculosis]).
  2. Causes of ambiguous genitalia:

5-alpha-reductase deficiency.
Androgen-secreting tumours.
Congenital adrenal hyperplasia.

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13
Q

what are the causes of secondary amenorrhea

A

1.hypothalamic-pituitary ovarian causes: most common

mainly causes by stress, increase in exercise and weightloss

  • The female athlete triad : low energy availability menstrual dysfunction, and low bone density e.g. athletes - 40% of female athletes have amenorrhoea
    2. physiological causes:

pregnancy

lactation

menopause

  1. hyperprolactinaemia - 30% have galactorrhoea
  2. severe systemic disease e.g. renal failure, thyroid disease, pituitary disease and haemochromatosis
  3. Polycystic ovarian syndrome - common
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14
Q

how do you diagnose amenorrhea?

A

Examine:

  1. Measure height and body weight, and calculate body mass index (BMI) for weight-related causes of amenorrhoea
  2. Turner’s syndrome features (short stature, web neck, shield chest with widely spaced nipples, wide carrying angle, and scoliosis).
  3. Features of Cushing’s syndrome features (striae, buffalo hump, significant central obesity, easy bruising, hypertension, and proximal muscle weakness).
  4. Hirsutism and acne (suggesting PCOS, especially in those with a high BMI).

testing

  1. βhcg e.g. urinary - excludes pregnancy
  2. FSH/LH - will be low in hypothalamic-pituitary causes but may be normal if weight loss or excessive exercise is the cause. will be raised
  3. Prolactin - increased by stress, hypothyroidism,prolactinomas and drugs
  4. Genetics - karotyping for turners
  5. Thyroid function tests
  6. tesosterone level - will be raised in androgen secreting tumor

Imaging:

MRI head for suspected pituitary tumour

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15
Q

how do you manage amenorrhea?

A
  1. manage the underlying cause
  2. lifestyle changes - applies to secondary amenorrhea caused by weight loss, excessive exercise, stress, or chronic illness
  3. contraception pills - as ovulation may occur at any time
  4. assisted conception if she wants to be pregnant
  5. manage risk for osteoporosis:

For women with premature ovarian failure (younger than 40 years of age), hypothalamic amenorrhoea, or hyperprolactinaemia (women with amenorrhoea associated with low oestrogen levels who are at increased risk of developing osteoporosis):

Treat the underlying cause, if possible.
Assess their fragility fracture risk.

Advise maintaining a healthy lifestyle to optimize bone health. This involves doing weight-bearing exercises, avoidance of smoking, eating a balanced diet, and maintenance of normal body weight.

Correct vitamin D deficiency, and ensure an adequate calcium intake.

Consider offering hormone replacement therapy (HRT) or the combined oral contraceptive (COC) pill (both off-label use) if amenorrhoea persists for more than 12 months.

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16
Q

what is polycystic ovarian syndrome (PCOS)?

A

consists of:

hyperandrogenism

oligomenorrhoea

polycystic ovaries on Ultrasound

cause is unknown

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17
Q

what is polycystic ovarian syndrome associated with?

A

obese

metabolic syndromes - hypertension, dyslipidaemia, insulin resistance, and visceral obesity

higher prevalence of T2DM and sleep apnoea

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18
Q

how do you diagnose Polycystic ovarian syndrome?

A

Rotterdam criteria (2 out of 3 must be present) :

  1. polycystic ovaries (12 or more follicles or ovarian volume >10cm3 on US)
  2. oligo-ovulation or anovulation
  3. clinical and/or biochemical signs of hyperandrogenism

same diagnosis as amenorrhea

imaging - pelvic ultrasound

oral glucose tolerance - for T2DM

fasting lipid panel

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19
Q

how do patients with PCOS present?

A

oligomenotthea with or without hirsutism, acne and subfertility

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20
Q

How do you manage PCOS?

A

Lifestyle management - weight loss and exercise are the mainstay of treatment and increase insulin sensitivity (metformin).

encourage smoking cessation

monitor + manage for - diabetes, hypertension,dyslipidaemia and sleep apnoea

fertility management:

clomifene citrate - induces ovulation

metformin as an alternative to clomifene- may improve menstrual disturbance and ovulatory function but does not have a significant on hirsutism or acne

use ovarian drilling if patient is not reacting to clomifene

gonadotrophins

IVF

hirsutism - treated cosmetically or with antiandrogen e.g. cyproterone

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21
Q

what are the causes of menorrhagia

A
  1. dysfunctional uterine bleeding (DUB) - heavy/ irregular bleeding without the absence of recognizable pelvic pathology - diagnosis of exclusion
  2. IUCD
  3. fibroids
  4. endometriosis
  5. adenomyosis
  6. pelvic infection
  7. polyps
  8. hypothyroidism
  9. coagulation disorders
  10. increasing age
  11. cooper coil
  12. endometrial cancer
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22
Q

what are the signs and symptoms of menorrhagia?

A

heavy prolonged vaginal bleeding

often worse at the extremes of reproductive life

dysmenorrhoea

symptoms of anaemia, pallor

enlarged uterus - suggests fibroids or adenomyosis

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23
Q

how do you diagnose menorrhagia?

A

exclude pregnancy

PV exam

Bloods: FBC, TFT, LFT, coagulation screen

Imaging:

US first line

hysteroscopy and endometrial sampling

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24
Q

how do you manage menorrhagia?

A

fibroids less than 3 cm in diameter, or suspected or diagnosed adenomyosis:

A LNG-IUS - first-line treatment e.g. mirena IUS

  1. pharmacological treatment should be considered: non-hormonal

tranexamic acid

nonsteroidal anti-inflammatory drug

hormonal

combined hormonal contraception

cyclical oral progestogens

  1. Secondary care treatment : pharmacological options not already tried, uterine artery embolization,

surgery

myomectomy

hysterectomy

second-generation endometrial ablation

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25
Q

what is premenstrual syndrome (PMS)?

A

condition which manifests with distressing physical, behavioral and psycho social symptoms in the absence of organic or psychiatric disease, regularly occuring during the luteal phase of the menstrual cycle.

significant improvement by the end of menstrual cycle

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26
Q

what are the signs and symptoms of PMS?

A

mood swings

irritability

depression

bloating

breast tenderness

headache

reduced

visuospatial ability

increase in accidents

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27
Q

how do you diagnose PMS?

A

physical examinatio indicated by the woman’s age and routine gynaecological and medical recommendations

patient record daily symptom diary for two or three cycles

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28
Q

how do you manage PMS

A
1. Offer lifestyle advice that includes:
Regular, frequent (2–3 hourly), small, balanced meals rich in complex carbohydrates.
Regular exercise.
Regular sleep.
Stress reduction.
Smoking cessation (if applicable).
Alcohol restriction (if applicable).
  1. if the predominant symptom is pain (for example headache or generalized aches and pains), prescribe a simple analgesic
  2. For women with moderate PMS symptoms:
    Consider prescribing a new-generation combined oral contraceptive (COC)

CBT

  1. for women with severe PMS:
    Consider prescribing a selective serotonin reuptake inhibitor (SSRI)
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29
Q

what is the menopause?

A

time of waning fertility leading up to the last period.

it is a retrospective diagnosis having said to have 12 months after the last perioid

average age is 52 yrs

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30
Q

what is peri-menopause?

A

transition phase from pre to post menopausal and the time in which symptoms are experienced.

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31
Q

what are the symptoms of menopause?

A
  1. Hot flushes/night sweats (vasomotor symptoms)
  2. Cognitive impairment and mood disorder
  3. Urogenital symptoms (genitourinary syndrome of menopause)
  4. Altered sexual function
  5. Sleep disturbance
  6. atropy of oestrogen- dependent tissues (genitalia, breasts) and skin
  7. vaginal atrophy - atrophic vaginitis
  8. osteoporosis
  9. increased risk of cardiovascular and cerebrovascular disease
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32
Q

how do you diagnose the menopause?

A
  1. clinical

2. investigation 2 consecutive: FSH level (more than 30 IU/L)

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33
Q

how do you manage the menopause?

A
  1. diet and exercise can relieve symptoms
  2. Hormone replacement therapy (HRT)
  3. vaginal dryness - oestrogen cream
  4. menorrhagia responds to mirena coil
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34
Q

what are the main routes of administration of Hormone replacement therapy?

A
  1. oral
  2. transdermal patch
  3. injection
  4. intra uterine (mirena)
  5. intra vaginal (pessary ring)
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35
Q

when do you prescribe oestrogen only HRT?

A

Oestrogen-only preparations are given to women without a uterus

unopposed oestrogen is a risk factor for endometrial cancer

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36
Q

when do you prescribe combined HRT?

A

combined oestrogen and progestogen preparations are given to women with an intact uterus

routes - oral, patch, mirena coil

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37
Q

what type of HRT do you prescribe for women who are having periods, or who are 12 months of a period? (perimenopausal)

A

Oestrogen and cyclical progestogen

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38
Q

what type of HRT do you prescribe for postmenopausal woman ?

A

monthly or 3-monthly cyclical regimens, or a continuous combined regimen may be used.

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39
Q

what are the adverse effects of HRT?

A

Oestrogen-related adverse effects: Fluid retention, bloating, breast tenderness or enlargement, nausea, headaches, leg cramps, dyspepsia, oestrogen-dependent cancer

Progestogen-related adverse effects: Fluid retention, breast tenderness, headaches or migraine, mood swings, premenstrual syndrome-like symptoms, depression, acne vulgaris, lower abdominal pain, and back pain.

Venous thromboembolism (VTE)

Vaginal bleeding problems - common

dementia

endometrial cancer - risk only seeen in use of oestrogen only in women

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40
Q

what are the benefits of HRT?

A
  1. reduction of vasomotor symptoms
  2. improvement in urogential symptoms and sexual
  3. reduced risk of colorectal cancer
  4. prevention and treatment of osteoporosis
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41
Q

what is the latest date for a termination?

A

24 weeks unless for medical reasons

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42
Q

what are the 2 main common grounds for termination of pregnancy?

A
• CLAUSE C – up to 23+6 weeks
“the pregnancy has not exceeded its
24th week and the continuance of the
pregnancy would involve risk, greater
than if the pregnancy were terminated,
of injury to the physical or mental health
of the pregnant woman”
• CLAUSE E – no gestational limit
“there is a substantial risk that if the
child were born it would suffer from
such physical or mental abnormalities
as to be seriously handicapped”
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43
Q

can a doctor refuse to carry out an abortion?

A

yes, HCPs the right to refuse to participate in abortion care

however it Limits are:
• Does not apply in emergency or life-threatening situations
• Should not delay or prevent a patient’s access to care
• Does not apply to ‘indirect’ tasks associated with abortion e.g. administrative,
supervision of staff etc

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44
Q

how do you carry out medical termination?

A

<9 weeks:

vaginal misoprostol only - prostaglandin analogue

advise them to contact doctor if bleeding hasn’t started in 24 hrs

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45
Q

what document certifies a termination and who signs it?

A

Certified on HSA1 form

(“Certificate A”) - 2 doctors sign

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46
Q

what categories of medical termination are there?

A

early - <9weeks

Late 9-13 weeks

mid trimester/late 13-24

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47
Q

how do you assess termination of pregnancy?

A

Clinical
• Estimated by LMP +/- date of +ve UPT
• Palpable uterus ( > 12 wks)

 Ultrasound
• Abdominal or transvaginal (< 6wks)
• Frequently used for all pre-COVID
• Now via risk assessment (~1/3)
• Symptoms or risk factors for ectopic
• Uncertainty about dates
• Before STOP in some areas
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48
Q

how is surgical method of termination of pregnancy is carried out?

A

Removal of pregnancy via surgical procedure (under anaesthesia)
• Cervical priming via misoprostol or osmotic dilators

< 14wks
• Electric vacuum aspiration (GA)
• Manual vacuum aspiration (up to 10wks; LA)

> 14wks
• Dilatation and evacuation

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49
Q

what are the contraindications of abortions?

A

Haemorrhage +/- blood
transfusion

Failed/incomplete
abortion

Infection

Uterine perforation
(surgical risk only)

Cervical trauma (surgical
risk only)
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50
Q

where are endometriotic deposits normally found?

A

in the pelvis

on the ovaries

peritoneum

uterosacral ligaments

pouch of Douglas

myometrium - this type of endometriosis is called adenomyosis

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51
Q

what is subfertility?

A

Infertility is defined as the period of time people have been trying to conceive without success after which formal investigation is justified and possible treatment implemented.

happens 1/7 couples

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52
Q

what are the main causes for infertility?

A
  1. Male factor (25%)
  2. anovulation (21%) - may be caused by premature ovarian failure, turner syndrome, surgery or chemotherapy, CPOS, excessive weight loss or weight loss
  3. tubal factor (15-20%)
  4. unexplained (28%)
  5. endometriosis (6-8%)
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53
Q

what are the risk factors of infertility

A

smoking

obesity

occupational risks

excessive alcohol consumption

drug use.

Female fertility declines with age; the effect of age on male fertility is less clear

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54
Q

what investigations can be carried out primary care for infertility?

A

unable to conceive after 1 year of regular unprotected sexual intercourse

men:

chlamydia screening

semen analysis - repeat in 3 months if abnormal

plasma FH is raised in testicular failure

karotype - exclude 47 xxy

female:

mid-luteal phase progesterone levels - in all women to confirm ovulation - day 21 progesterone >30nmol/L is indicative of ovulation

serum gonadotrophins levels - only with women who have irregular cycles

TFTS

prolactin measurement

chlamydia screening

rubella immunity

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55
Q

what imaging do you carry out for infertility

A

Transvaginal ultrasound

Hysterosalpingogram (HSG) uses x-ray and contrast injected through a small cannula in the cervix

laparoscopy and dye test - gold standard procedure for assessing tube patency but 2nd line to HSG or HYCOSY

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56
Q

what are the causes of female infertility?

A
  1. Ovulatory

Group I ovulation disorders: also known as hypogonadotrophic hypogonadism) are caused by hypothalamic pituitary failure e.g. hypothalamic amenorrhea and hypogonadotrophic hypogonadism

Group II ovulation disorders: dysfunctions of the hypothalamic-pituitary ovarian axis e.g. (PCOS) and hyperprolactinaemic amenorrhoea

Group III ovulation disorders caused by ovarian failure

hyperthyroidism and hypothyroidism

Cushing’s syndrome and congenital adrenal hyperplasia

  1. Tubal, uterine, and cervical factors:

STIs and PIDs

Endometriosis

Cervical mucus defect or dysfunction.

Submucosal fibroids

  1. Drugs

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Spironolactone

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57
Q

what are the causes of male infertility?

A
  1. Primary spermatogenic failure
e.g.
 Anorchia (absence of testes).
Testicular dysgenesis
Trauma.
Testicular torsion.
Post-inflammatory forms
varicocele
tumours
  1. Genetic disorders:

Klinefelter’s syndrome with karyotype 47, XXY

  1. Obstructive azoospermia (defined as the absence of both spermatozoa and spermatogenic cells in semen and post-ejaculate urine due to bilateral obstruction of the seminal ducts).

e.g. Ejaculatory duct obstruction
Vas deferens obstruction
Epididymal obstruction

  1. other:

erectile dysfunction

Sulfasalazine — can cause infertility and oligospermia

Androgens and anabolic steroids

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58
Q

what is the normal semen analysis?

A

semen volume - 1.4 ml

total sperm number (million per ejaculate) - 39

sperm concentration (million per ml) -16

total motility - 42

progressive motility -30

vitality -54

sperm morphology - 4%

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59
Q

what is azoospermia?

A

no sperm in ejaculate

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60
Q

what asethenozoospermia?

A

% progressive motile sperm below reference limit

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61
Q

what is oligozoospermia?

A

total number / concentration of sperm below reference limit

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62
Q

What is teratozoospermia?

A

% morphologically normal sperm below reference limit

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63
Q

what is oligoasthenozoospermia?

A

combination of: Asthenozoospermia (reduced sperm motility) and Oligozoospermia (low spermatozoon count)

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64
Q

oligoteratozoospermia?

A

combination of teratozoospermia and azoospermia

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65
Q

how do you manage subfertility?

A
  1. ovulation induction

A. clomifene citrate - 1st line
50-100-150 mg tab days 2-6

alternative is letrozole

B. gonadotrophin injections - recombinant FSH

can cause multiple pregnancy/ overstimulation

C. laparoscopic ovarian drilling

  1. surgical techniques

Tubal microsurgery in women with mild tubal disease

Surgical ablation, or resection of endometriosis plus laparoscopic adhesiolysis in women with endometriosis.

men:

Surgical correction of epididymal blockage in men with obstructive azoospermia

IVF

intrauterine insemination (IUI)

intracytoplasmic sperm injections (ICSI)

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66
Q

what is ovarian hyperstimulation syndrome?

A

complication of ovulation induction or superovulation. this is a systemic disease and vasoactive products are central to its pathophysiology

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67
Q

what are the characteristics of ovaria hyperstimulation syndrome?

A
  1. ovarian enlargement
  2. fluid shift from intravascular to extravascular space
  3. this leads to the accumulation of fluid in peritoneal and pleural spaces
  4. intravascular volume depletion causes haemoconcentration are hypercoagulability
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68
Q

what are the risk factors of ovarian hyperstimulation syndrome?

A

young age

Low BMI

polycystic ovaries

previous OHSS

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69
Q

what is the presentation of OHSS?

A
  1. abdominal discomfort
  2. nausea
  3. vomiting
  4. abdominal distention

usually lasts 3-7 days after hcg administration or 12-17 days if pregnancy has ensured

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70
Q

how do you manage OHSS?

A

mild - moderate:

analgesia - avoid NSAIDs

drink to thirst not to excess

avoid strenuous activities and intercourse due to risk of ovarian torsion

continue progesterone luteal support - avoid hCG

severe:

analgesia and antiemetics
check FBCs, LFTs. U&E and albumin

strict fluid balance

check for ascites and thrombosis

urinary catheter

thromboprophylaxis with compression stockings and LMWH

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71
Q

what is a prolapse?

A

occurs when the weakness of the supporting structures allows the pelvic organs to protrude within the vagina.

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72
Q

what types of prolapses are there?

A

cystocele: anterior wall of the vagina and the bladder attached to it, bulge
urethrocele: lower anterior wall is location of lump. v similar to cystocele

Rectocele: lower posterior wall which is attached to rectum may bulge through weak levator ani.

enterocele - bulges of the upper posterior vaginal wall may contain loops of intestine from the pouch of Douglas.

uterine prolapse : protrusion of the uterus downwards into the vagina, taking with it the cervix and upper vagina.

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73
Q

how do you grade prolapses?

A

1st degree - lowest part of the prolapse descends halfway down the vaginal axis to the introitus

2nd degree - lowest part of the prolapse extends to the level of the introitus and through the introitus on straining

3rd degree: lowest part of the prolapse extends through the introitus and outside the vagina.

Procidentia: refers to 4th degree uterine prolapse - uterus lies outside the vagina

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74
Q

what are the risk factors of prolapse?

A
  1. congenital
  2. prolonger labour
  3. trauma from instrumental delivery
  4. lack of postnatal pelvic floor exercise
  5. obesity
  6. chronic cough
  7. constipation
  8. smoking
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75
Q

what are the symptoms of prolapse?

A
  1. can be asymptomatic
  2. dragging sensation
  3. discomfort
  4. sensation o heaviness or pulling in the vagina
  5. feeling of a lump coming down
  6. dyspareunia - painful intercourse
  7. backache
  8. urinary incontinence or retention
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76
Q

what investigations do you carry out for prolapses?

A
  1. Bimanual to exclude pelvic masses
  2. Pelvic organ prolapse quantification system (POP-Q)

patient straining - 6 specific sites are evaluated

patient at rest - 3 sites

measure each site in relation to the hymenal ring. if a site is above the hymen then give a negative number

if a site is below the hymen then give a positive number

  1. urodynamic studies if urinary continence
  2. pelvic ultrasounds
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77
Q

how do you manage prolapses?

A
  1. conservative:

avoid heavy lifting

lose weight

stop smoking

vaginal oestrogens: only if symptomatic atrophic vaginitis

Pessaries:

useful for women unfit for surgeries.

Relief symptoms whilst awaiting surgery

further pregnancies planned or pregnant

diagnostic test for prolapse

  1. surgery:

Cystocele/ uretrocele - anterior colporrhaphy

Rectocele/ entereocele - posterior colporrhaphy

uterine/ vaginal vault - sacrospinous ligament fixation or hysterectomy

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78
Q

give example of contraception methods.

A
  1. combined pill (hormonal method)
  2. condoms (barrier method)
  3. DMPA injection
  4. patch (hormonal method)
  5. contraceptive implant (hormonal method)
  6. copper coil (intrauterine method)
  7. diaphragm (barrier methods)
  8. IUS (intrauterine method)
  9. The ring (hormonal method)
  10. mini pill (hormonal method)
  11. surgical sterilisation (permanent method)
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79
Q

what are the three types of mechanisms for contraception?

A
  1. prevention of ovulation
  2. prevention of fertilisation
  3. prevention of implantation
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80
Q

Give examples of Long acting reversible contraception (LARC)?

A
  1. IUS
  2. IUD either levo
  3. Nexplanon
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81
Q

What is the mechanism of LARC?

A

prevention of ovulation

apart from hormone coil and traditional Progesterone only pill

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82
Q

how long do LARCs provide contraceptive cover for?

A

12-14 weeks

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83
Q

what are the contraindications for LARC?

A
  1. Pregnancy
  2. Breast cancer
  3. severe cardiac disease
  4. undiagnosed vaginal bleeding
  5. submucosal fibroids
  6. uterine malformation
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84
Q

what are the side effects of LARC?

A

weight gain

increased risk of osteoporosis

risk factor for ectopic pregnancy

delay in return of fertility

irregular bleeding

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85
Q

What is a VLARC?

A

very long acting resisting contraceptive

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86
Q

give an example of a VLARC?

A

Copper coil - non hormonal IUD

IUS: mirena coil

Implant

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87
Q

what is the mechanism of action for copper coil?

A

prevention of fertilisation

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88
Q

how long does a copper coil stay in the uterus for?

A

5-10 years

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89
Q

what are contraindications for copper coils?

A

peptic ulcer disease

current pelvic infection

abnormal uterine anatomy

history or current endometrial or cervical cancer

pregnancy - increased risk of ectopic pregnancy and second trimester miscarriage

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90
Q

when should you insert a copper coil ?

A

first 7 days of period

anytime if reasonably certain they are not pregnant

up to 5 days UPSI for emergency contraception

immediately after termination of pregnancy

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91
Q

what are the side effects copper coil?

A

Side effects: heavy, prolonged periods

problems with insertion: pain, increased risk of infection, uterine perforation, expulsion of device

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92
Q

what type of mechanism of action does the IUS have?

A

prevention of implantation

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93
Q

how long can a IUS be used for?

A

3- 5 years insertion

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94
Q

what are the contraindications of IUS?

A

peptic ulcer disease

current pelvic infection

abnormal uterine anatomy

history or current endometrial or cervical cancer

pregnancy - increased risk of ectopic pregnancy and second trimester miscarriage

not used as a method of emergency contraception

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95
Q

when is an IUS suitable for insertion?

A

within first 7 days of period

<48 hrs or >4 weeks post partum

immediately after termination of pregnancy

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96
Q

What is the mechanism of action for the implant?

A

inhibition of ovulation

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97
Q

how long does the implant stay in the body for?

A

3 years - needs to be changed more regularly if obese

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98
Q

when should you put an implant in?

A
  1. within first 5 days of cycle
  2. on or before day 21 post partum
  3. up to 5 days post first or second trimester abortion
  4. starting after last active pill taken
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99
Q

when will condom cover be required for implants?

A

started an other time in the cycle

used a s a quick start for emergency contraception

switching from POP, mirena, IUD

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100
Q

what are the side effects of Implants?

A

irregular bleeding, weight gain, acne

problems with insertion: nerve damage and pain on insertion

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101
Q

what do short acting combined hormonal contraception contain?

A

both oestrogen and progesterone

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102
Q

what is the mechanism of action for short acting combined hormonal contraception?

A

inhibition of ovulation

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103
Q

give examples of short acting combined hormonal contraception?

A

transdermal patch

combined oral contraceptive pill

short acting single hormonal contraception

vaginal ring

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104
Q

how does the transdermal patch last for?

A

single patch is applied for one week at a time for three weeks

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105
Q

what are the problems for transdermal patch?

A

if the woman is obese it reduces efficacy

breast pain, nausea and painful periods more common than with other combined preparations

increased thrombotic risk

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106
Q

How long does a vaginal ring last for?

A

21 days

followed by a 7day ring free period

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107
Q

How long do you need to take a combined oral contraceptive pill for?

A

pill taken for 21 consecutive days

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108
Q

when do you start taking the contraceptive pill?

A

if taken on first 5 days of cycle - no cover required

if taken after first 5 days of cycle - 7/7 condoms

emergency contraception: immediately after levonelle, 5 days after ellaone

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109
Q

what are the side effects of contraceptive pill?

A

vomiting - take again if this happens within 2 hours

diarrhoea - take again if this happens within 24 hrs

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110
Q

what happens if they miss taking a pill between 24<48 hrs?

A

take missed pill and continue with rest of pack as normal

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111
Q

what happens if you miss 2 pills >48 hrs

A

week 1 - take most recent pill use 7/7 condom cover and consider emergency contraception

week 2: take most recent pill, 7/7 condom cover

week 3: take most recent pill, 7/7 condom cover and omit break

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112
Q

what happens if you miss >2 pills?

A

emergency contraception if in first week

continue with rest of the pack and omit break

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113
Q

what are the benefits of combined pill?

A

improves acne

improves pre menstrual symptoms

protects against ovarian, endometrial and colorectal cancer

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114
Q

what are the side effects of combined pill?

A
  1. increased VTE
  2. increased CVD and stroke risk
  3. increased risk of breast and cervical cancer
  4. increased BP
  5. mood swings
  6. nausea and vomiting
  7. irregular bleeding
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115
Q

what are the contraindications for combined pill?

A
  1. migraine with aura- recurring headache that strikes after or at the same time as sensory disturbances called aura.
  2. smoking >15 cigarettes if >35 yo
  3. history of breast cancer
  4. anti phospholipid syndrome
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116
Q

what is a progesterone only pill?

A

pill which only contains progesterone e.g. etonogestrel or levenogestrel

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117
Q

what is the mechanism of action for POP?

A

thickens cervical mucus

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118
Q

how many times do you take POP?

A

take pill everyday at same time

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119
Q

when do you prescribe POP?

A

to women who are usually contraindicated for combined one

  1. breast feeding

> 35 and smoking

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120
Q

what are the side effects of POP?

A

DUB

Weight gain

headaches

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121
Q

where is incontinence in women maintained in the body?

A

urethra by the external sphincter and pelvic floor muscles

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122
Q

what is incontinence?

A

involuntary leakage of urine which is divided into urge, stress and mixed urinary incontinence

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123
Q

what is continuous urinary leakage most commonly associated with?

A

vesicovaginal fistula or congenital abnormality e.g. ectopic ureter

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124
Q

what investigations do you carry out for incontinence?

A

Urinalysis

Imaging - use US to exclude incomplete bladder emptying and define any pelvic mass . NOT routinely used however

cystoscopy - used to visualise urethra bladder,mucosa, trione and ureteric orifices. Biopsies can be taken

urodynamics - a combination of tests which lok at the ability of bladder to store and void urine. Uroflowmetry screens for voiding difficulties.

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125
Q

What is stress urinary incontinence? (SUI)

A

involuntary leakage of urine on effort or exertion, or on sneezing or coughing

mainly due to urethral sphincter weakness

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126
Q

what is urge urinary incontinence?

A

is the involuntary leakage of urine with a strong desire to pass urine.

commonly coexists with frequency and nocturia and forms overactive bladder syndrome

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127
Q

What is mixed urinary incontinence?

A

is the combination of stress and urge incontinence and usually one symptom will predominate (treat that first)

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128
Q

what is overflow incontinence?

A

usually due to injury or insult

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129
Q

what is the main common type of incontinence in women?

A

stress urinary incontinence

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130
Q

what is the pathophysiology of stress urinary incontinence?

A

when detrusor pressure exceeds the closing pressure of the urethra

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131
Q

what investigations do you carry out for stress urinary incontinence?

A

Exclude UTI

A frequency/ volume chart shows normal frequency and functional bladder capacity

urodynamics when surgery is considereed

check for detrusor overactivity

check for voiding dysfunction - woman with poor flow rate is at risk fo long - term urinary retention

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132
Q

what are the risk factors of SUI?

A

vaginal delivery

oestrogen deficiency from menopause

radiotherapy

congenital weakness

trauma from radical pelvic surgery

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133
Q

how do you manage SUI?

A

Lifestyle advise - weight loss, smoking cessation, treatment of chronic cough

Pelvic floor exercise (muscle training) for at least 3 months

Surgery:

Peri urethral injections of bulking agents

if they reject surgery then - duloxetine

tension- free vaginal tapes

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134
Q

What is overactive bladder syndrome (OAB)?

A

chronic condition affecting women and implies underlying detrusor overactivity (DO)

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135
Q

what are the causes of OAB?

A

incidence increases with age

idiopathic - main cause

rare caues:

MS

spina bifida

secondary to pelvic or incontinence surgery

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136
Q

what can provoke symptoms of OAB?

A

cold weather

opening the front door

coughing

sneezing

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137
Q

what are the symptoms of OAB?

A

stress incontinence symptoms

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138
Q

how do you diagnose OAB?

A

detrusor overactivity - diagnosed via urodynamic testing

exclude UTI

frequency/ volume chart typically shows increased diurnal frequency and nocturia

urodynamics shows involuntary detrusor contractions during filling - done when there is a doubt about diagnosis

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139
Q

how do you manage OAB?

A

bladder retraining

pharmacology:

anticholinergics e.g. oxybutynin, solifenacin or mirabegron

side effects include dry mouth, constipation and nausea

intravaginal oestrogen cream can help in those with vaginal atrophy

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140
Q

what are the causes of vulval lumps?

A

local varicose veins

boils

sebaceous cysts

bartholins cyst or abscess

uterine prolapse or polyp

inguinal hernia

varicocele

carcinoma

viral warts

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141
Q

what are vulval warts?

A

genital warts caused by HPV

spread via sexual contact

incubation is weeks

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142
Q

what body parts can be affected by vulval warts?

A

vulva

perineum

anus

vagina

cervix

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143
Q

which HPV causes vulval warts?

A

HPV 6 and 11

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144
Q

which HPV causes vulval and cervical intraepithelial neoplasia?

A

16,18 and 33

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145
Q

what can vulval warts cause?

A

anal carcinoma

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146
Q

how do you manage vulval warts?

A

warts can be destroyed via the following:

cryotherapy

trichloroacetic acid

electrocautery

only treat a few warts at a time to avoid toxicity

self application:

podophyllotoxin cream

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147
Q

what type of cancers can HPV 6 and 11 may cause in offspring of affected mothers with vulval warts??

A

laryngeal or respiratory papilomas

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148
Q

what is urethral caruncle?

A

This is a small red swelling at the urethral orifice.

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149
Q

what is the main cause of urethral caruncle?

A

meatal prolapse

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150
Q

when can urethral caruncle cause pain?

A

on micturition

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151
Q

how do you manage urethral caruncle?

A

excision or diathermy

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152
Q

what is a bartholin’s cyst and abscess?

A

if the bartholin’s duct and glands are blocked a painless cyst forms however if this becomes infected it can become extremely painful - basically cannot sit down

a hot red labium is seen

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153
Q

how do you manage bartholin’s cyst and abscess?

A

abscess should be incised and permanent drainage ensured by marsupialisation

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154
Q

what tests might you do for batholin’s cyst and abscess?

A

exclude gonococcus

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155
Q

what is vulvitis?

A

vulval inflammation may due to infections e.g. candida, herpes simplex, chemicals

often associated with vaginal discharge

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156
Q

what are the causes of vulval ulcers?

A

syphilis - main cause

herpes simplex - common in young

carcinoma

chancroid

TB

Behcet syndrome

crohns disease

granuloma inguinale

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157
Q

what is herpes simplex?

A

Herpes is an enveloped DNA virus.

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158
Q

what types of herpes are there?

A

HSV 1

HSV 2

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159
Q

which herpes causes genital infection?

A

both do

HSV 2 more common though

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160
Q

what is the primary infection of Herpes simplex?

A

usually the most severe

starts with the prodrome (itching of affected skin)

flu- like illness

progresses to vulvitis pain and small vesicles on the vulva

urinary retention may occur due to autonomic nerve dysfunction

recurrent attacks are usually less severe and may be triggered by illness, stress, sexual intercourse and menstruation

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161
Q

how do you manage herpes simplex?

A

strong analgesia

lidocaine gel

anti viral - aciclovir orally shorten symptoms. dont give topical cream

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162
Q

what is the clinical presentation of carcinoma of the vulva?

A

lump : as an indurated ulcer which may not be noticed unless it causes pain and bleeding hence often presenting late

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163
Q

how do you manage carcinoma of the vulva?

A

depends on size of tumor

if <2cm wide and <1mm deep then lymph node excision is not needed

if >1mm deep do triple incision surgery = wide

radiotherapy may be used preoperatively to shrink tumours if sphincters are affected

chemoradiation is used in people unsuitable for surgery to shrink large tumours preoperatively and for relapses

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164
Q

what are the signs and symptoms of cervical cancers?

A

cervical smear showing invasion

incidental finding on treatment of CIN

postcoital and or postmenopausal bleeding watery vaginal discharge

advance disease includes:

heavy vaginal bleeding

ureteric obstruction

weight loss

bowel disturbance

vesicovaginal fistula

pain

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165
Q

what would you see when examining the cervix if there was cervical cancer?

A

colposcopy shows an irregular cervical surface abnormal vessels and dense uptake of acetic acid

bimanual examination:

the cervix feels roughened and hard and if disease is advanced there is loss of the fornices and the cervix is fixed

speculum examination:

shows an irregular mass that often will bleed on contact

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166
Q

what investigations should you do for cervical cancer?

A

FBC , U&E LFTs Punch biopsy for histology

large loop excision of the transformation zone (LLETZ) is contraindicated

CT abdomen and pelvis for staging

MRI pelvis helps with staging and identifying lymph nodes

examination under anaesthetic helps staging

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167
Q

what are the causes of cervical cancer?

A

HPV 16 and 18 are main causes

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168
Q

what are the risk factors of cervical cancer?

A

HPV particularly 16 and 18

inadequate cervical screening

  1. risk of HPV infection depends on:

number of sexual partners

age at first sexual intercourse

no condom use

  1. woman with HPV the following factors increase risk of progression to cervical cancer

other STIs e.g. herpes simplex, chlamydia or gonococcal infections

smoking

high parity

family history in a first degree relative

oral contraceptive pill for longer than 5 years

  1. immunosuppresed women
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169
Q

how do you manage cervical cancer?

A

1.prevention

NHS screening (offered 25 - 640

HPV vaccination - girls at 12-13

use of condoms

  1. Management

depends on stage:

  1. CIN

colposcopy

biopsy and histological analysis

moderate to severe abnormalities are found: excision or ablation

  1. Stage IA1 (microinvasive disease)

conservatively - no need for lymphadenectomy

  1. Stage IA2 (early stage disease)

tumour <4cm - radical hysterectomy with lymphadenectomy

Tumour >4cm - chemoradiation

  1. Stage IIB (locally advanced disease)

chemoradiation

  1. Stage IVB (metastatic disease)

combination chemotherapy is the treatment of choice

single agent therapy and palliative care also option

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170
Q

what is cervical intraepithelial neoplasia (CIN)?

A

precursor lesion of invasive carcinoma

diagnosis is made via biopsy

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171
Q

what is a dyskaryosis

A

cytological term used to describe cervical smears

the change of appearance in cells that cover the surface of the cervix

high false positives and negatives so colposcopy is required

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172
Q

what is colposcopy?

A

examination of the cervix via a colposcope

two stains are used : iodine or acetic acid

Iodine - abnormal areas don’t change colour

Acetic acid - abnormal areas turn white

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173
Q

what do you do if there is high grade colposcopy?

A

suggests CIN II - III therefore intervene

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174
Q

do colposcopy detect adenocarcinomas of the cervix?

A

nope

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175
Q

define CIN I,II,III

A

CIN I - 1/3rd of the thickness of the cervical surface layer is affected. Regresses spontaneously in 60% of cases with no treatment

CIN II- 2/3rds of the thickness of the surface layer is affected. progresses to cancer in 5% of cases

CIN III - high grade dysplasia. full thickness of the surface layer is affected 20-30% of cases in CIN III progress to cervical cancer.

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176
Q

how do you manage CIN?

A

LLETZ - large loop excision of the transformation zone

occurs with colposcopy clinic local anaesthetic using loop diathermy - 90% cure rates in one treatment

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177
Q

what is CGIN?

A

cervical glandular intraepithelial neoplasia it can coexist with CIN or be a sole finding

difficult to manage as the endocervical epithelium extends into the cervical canal and therefore not completely visible at colposcopy

associated with high risk HPV and higher skip lesions

manage with cylindrical LLETZ ,cone biopsy or hysterectomy if she doesn’t want kids

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178
Q

what are the stages of cervical cancer?

A

stage I - tumours confined to cervix :1A microscopic 1B macroscopic

Stage 2 - have extended locally to pper 2/3 of the vagina IIb to parametria

Stage 3 - spread to lower 1/3 of vagina IIIa or pelvic wall

stage 4 - spread to bladder or rectum 1

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179
Q

how common are vaginal cancers?

A

extremely rare <1% of gynaecological malignancies

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180
Q

what is the clinical presentation of vaginal cancers?

A

most are squamous in origin

usually in older women

commonest in the upper 1/3rd of vagina

bleeding

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181
Q

how do you manage vaginal cancers?

A

radiotherapy

prognosis is poor

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182
Q

what is the cause of endometrial cancer?

A

related to excessive exposure to oestrogen unopposed to progesterone

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183
Q

what are the risk factors for endometrial cancer?

A
  1. obesity
  2. T2DM
  3. hypertension
  4. nulliparity
  5. anovulatory cycles e.g. PCOS
  6. early/late menopause
  7. HNPCC (lynch II syndrome) gene
  8. oestrogen only HRT
  9. breast cancer
  10. combined pill
184
Q

What is the clinical presentation of endometrial cancers?

A
  1. older woman
  2. post menopausal bleeding (PMB)
  3. vaginal discharge
  4. pyometra
  5. Thrombocytosis
  6. haematuria
185
Q

how do you diagnose Endometrial cancer?

A
  1. PMB is early sign
  2. visible haematuria and low haemoglobin levels
  3. thrombocytosis
  4. high blood glucose levels

transvaginal ultrasonography (TVS) shows endometrial thickness >4mm then maybe suggestive

Biopsy via outpatients or with hysteroscopy

use CT for assessing distance metastases in those proven to have advanced local disease

MRI - investigation of choice to stage pelvic disease

186
Q

what is the staging of endometrial cancer?

A

stage I - body of the uterus only

II - body and cervix only

III - beyond the uterus but not the pelvis

IV - extends beyond the pelvis

187
Q

how do you manage endometrial cancer?

A

Surgical:

total hysterectomy + bilateral salpingo-oophrectomy

medical:

external beam radiotherapy - used as palliative treatment in those who cant have surgery

vaginal brachytherapy - is used to post op to reduce recurrence

external beam radiotherapy

oral progesterone

chemotherapy

all depends on stage

stage 1 - surgery +/- radiotherapy

stage 2 - surgery +/- radiotherapy

stage 3 - maximal debulking surgery + lymph node dissection + radiotherapy

stage 4 - maximal debulking surgery + palliative radio/chemotherapy

188
Q

what is the pathophysiology of benign ovarian tumours?

A

can be physiological due to follicular cysts or corpus luteal cysts

epithelial tumours - serous and clear cell

germ cell (mesoderm) tumours - mature teratoma, dermatoid cyst

fibroma - meigs syndrome - ovarian fibroma + ascites +PE

189
Q

what would benign ovarian tumours be like on examination?

A

irregular looking ovaries

may be normal if cyst is small or woman is obese

abdominal examination:

mass arising from the pelvis, tenderness, peritonism or ascites

vaginal examination:

vaginal discharge or bleeding, cervical excitation, adnexal mass, or tenderness

nodular uterosacral ligaments and a fixed retroverted uterus —- endometriosis

ovarian torsion is uncommon :

presents with severe lower abdominal pain and vomiting

deep seated colicky abdominal pain

fever may be in a minority

whirlpool sign ( free fluid on US)

190
Q

what imaging do you do for benign ovarian tumours?

A

TVS - good at distinguishing benign from malignant mass

transabdominal US for cyst extending out of pelvis

MRI and CT used in staging

191
Q

how do you manage benign ovarian tumours?

A

same as ovarian cysts

192
Q

what is a ovarian functional cyst?

A

enlarged or persistent follicular or corpus luteum cysts

usually resolve after 2-3 cycle

can be painful if rupture

193
Q

what is an endometriomas

A

ovarian cysts filled with old blood also known as chocolate cyst

194
Q

what is a ovarian serous cystadenomas?

A

neoplasms which are commonest in women aged 30-40

30% become cancerous

most common type of epithelial cell tumour

195
Q

what is a mucinous cystadenoma?

A

commonest large ovarian tumours

filled with mucinous material

remove appendix with suspected mucinous cystadenoma and send for histology

ruptures may cause pseudomyxoma peritonei

196
Q

what is a fibroma?

A

these are small, solid, benign, fibrous tissue tumours

associated with meigs syndrome: PE , often right sided + benign ovarian fibroma + ascites

197
Q

what is an ovarian teratoma?

A

tumour which arise from primitive germ cells

contain well differentiated tissue ( hair, teeth)

20% are bilateral

most common in young women

198
Q

what types of ovarian cancers are there?

A

epithelial - most common

Non epithelial:

germ cell tumours

ovarian carcinosarcoma

sex cord tumour

stromal tumour

small cell

neuroendocrine

squamous cell carcinoma

199
Q

where do secondary metastatic tumours in the ovary mostly come form?

A

endometrium

breast

GI tract

200
Q

what are the risk factors for ovarian cancer?

A

older women

smoking

obesity

BRCA 1 and BRCA 2 gene

family history of ovarian cancer

family history of breast cancer

nulliparity

early menarche

late menopause

IVF

HRT

201
Q

what are the signs and symptoms of ovarian cancer?

A

woman over 55

abdominal bloating

feeling full and/or loss of appetite

pelvic or abdominal pain

increased urinary urgency

weight loss

malaise or fatigue

change in bowel habit

202
Q

how do you diagnose ovarian cancer?

A

bloods

Serum CA125 - raised ( greater than 35 IU/ml) . not specific though

AFP, LDH and hCG too

examination:

Abdominal and pelvic examinations - may have ascites or a pelvic or abdominal mass ( make sure not uterine fibroids)

Imaging:

TVs or abdominal US first line

staging: CT CAP

Tissue sampling:

Ascitic tap - for cytology

staging surgery - laparotomy or laparoscopy for biopsy

203
Q

what are the stages of ovarian cancer?

A

Stage 1 limited to one or both ovaries

stage 2 limited to pelvis

Stage 3 limited to abdomen, including regional lymph node metastases

Stage 4 - distant metastases outside abdominal cavity

204
Q

how do you manage ovarian cancer?

A

surgery:

EARLY STAGES - OPEN HYSTERECTOMY, BSO ( bilateral salpingo oophorectomy and INFRACOLIC
OMENTECTOMY

LATE STAGES - RADICAL DEBULKING (Bring down disease burden to nil residual
disease).

if fertility required:

early disease can keep uterus and other ovary may be left

unilateral salpino-oophrectomy)

chemo: recommended in everyone following surgery unless disease is low grade 1a - 1b

platinum agents are best e.g. carboplatin with paclitaxel

205
Q

what type of epithelial ovarian cancers are there?

A
Serous 
Mucinous
Endometrioid
Clear cell 
Brenner
Undifferentiated carcinoma
206
Q

what is endometriosis?

A

presence of endometriotic tissue outside the uterus

hormone mediated

endometriotic deposits are mainly found in the pelvis, on the ovaries, peritoneum, uterosacral ligaments and pouch of douglas

207
Q

what is the cause of endometriosis?

A

unknown three main theories:

  1. retrograde menstruation
  2. metaplasia of mesothelial cells
  3. impaired immunity
208
Q

what are the signs and symptoms of endometriosis?

A

chronic pelvic pain

period related pain (dysmenorrhoea)

deep pain during or after sexual intercourse

period related GI symptoms e.g. painful bowel movements

period related urinary symptoms e.g. haematuria and pain passing urine

subfertility

can be asymptomatic

209
Q

how do you diagnose endometriosis?

A

Diagnostic:

gold standard - laparoscopy with biopsy

Examination:

abdominal and pelvic exam - look for abdominal masses and reduced organ mobility and enlargement

imaging:

transvaginal ultrasound

serum CA 125 may be raised can be normal though

210
Q

how do you manage endometriosis?

A

1.symptomatic relief:

NSAIDs for pain

  1. hormonal therapy : reduces endometriosis related pain. obvs dont give to women who want babies

Combined pill

POP

Mirena coil

COCP

GnRH analogues

  1. surgical management:

laparoscopy with ablation or excision

nodules should be excised rather than drained otherwise high recurrence

hysterectomy is indicated ( adenomyosis or heavy menstrual bleeding that have not responded to other treatments) all visible endometriotic lesions should be excised at the time of hysterectomy. it is last resort

211
Q

what is an adenomyosis?

A

presence of endometrial tissue with the myometrium

212
Q

what are uterine fibroids?

A

most common benign tumour in women they are a mixture of smooth muscle cells and fibroblasts which form hard, round whorled tumours in the myometrium

213
Q

what are the risk factors of uterine fibroids?

A

mutation in the gene for fumarate hydratase

increasing age

early puberty

obesity

black ethnicity

family history

214
Q

what is the clinical presentation of uterine fibroids?

A

mainly asymptomatic

symptoms:

heavy menstrual bleeding

pelvic pain

abdominal distention

pelvic pressure

urine frequency or incontinence

subfertility

215
Q

how do you diagnose for uterine fibroids?

A

Pelvic examination:

firm, enlarged and irregularly shaped non-tender uterus

mass can be moved slightly from side to side

large tumours- central irregular mass can be palpated on transabdominal examination

imaging:

ultrasound used to measure uterine length

can also use hysteroscopy to measure to uterine length (>12 cm)

216
Q

how do you manage uterine fibroids?

A

if asymptomatic:

no further investigation or management once diagnosed unless there is a rapid growth (suggests malignancy)

symptomatic:

GnRH analogues: e.g. goserelin - monthly 3-6 months before surgery used to shrink them. not long-term option

Myomectomy - use different types depending on size and location. submucosal fibroids better removed hysteroscopically

uterine artery embolization (UAE): don’t give to women who want fertility

217
Q

what contraception do you give to women with fibroids?

A

without distortion of uterine cavity - all can be used

with distortion of uterine cavity:

barrier methods (condom)

Combined hormonal contraception (Pill)

POP

female sterilisation - depends on location and size of the fibroid

give HRT for women with no symptoms from fibroids

218
Q

what are the main sites of uterine fibroids?

A

intramural

subserosal

pedunculated

submucosal

219
Q

What is pelvic inflammatory disease (PID)?

A

infection of the upper genital tract.

220
Q

what are the causes of PID?

A

STIs e.g.

chlamydia trachomatis (main cause)

Neisseria gonorrhoeae

usually from ascending infection from the endocervix - caused by mycoplasma genitalium

Uterine instrumentation e.g. due to termination of pregnancy or insertion of intrauterine device

postpartum

appendicitis

anaerobes and endogenous bacteria e.g. haemophilus influenzae, gardnerella vaginalis

221
Q

what are the risk factors for PID?

A

young age (younger than 25)

early age of losing virginity

multiple sexual partners

recent new partner

222
Q

what are the signs and symptoms of PID?

A

lower abdominal pain (usually bilateral can be uni)

deep dyspareunia

abnormal vaginal bleeding e.g. postcoital

abnormal vaginal discharge as a result of associated cervicitis, endometritis or bacterial vaginosis

examination:

lower abdominal tenderness (bilateral usually)

adnexal tenderness

uterine tenderness

speculum examination - abnormal cervical or vaginal mucopurulent discharge

223
Q

how do you diagnose PID?

A
  1. High vaginal swab - to exclude other vaginal infections e.g. bacterial vaginosis and candidiasis
  2. test for STIs
    chlamydia: vulvo- vaginal swab or endocervical swab

FCU - sample can be collected if preferred

Gonorrhoea: vulovovaginal swab or NAAT

  1. ESR, C protein and leucocyte count

imaging:

US - helpful if an abscess is suspected but not helpful in uncomplicated PID

MRI/ CT scanning of the pelvis can be helpful in differentiating PID from alternative diagnoses but not routinely used.

224
Q

how do you manage PID?

A

screen woman for infections

trace sexual partners of the woman from the past 6 months

  1. Drug treatment

pain relief - ibuprofen or paracetamol

  1. Antibiotics

if gonococcal infection is low:

ceftriaxone (as a single IM), oral doxycycline+ Oral metornidazole

or

oral ofloxacin (twice daily) + oral metronidazole (twice daily)

if mycoplasma genitalium is positive:

moxifloxacin

if gonococcal risk is high:

ceftriaxone (single IM dose), followed by oral doxycycline (twice daily) + oral metronidazole (twice daily)

remember : ofloxacin and moxifloxacin or azithromycin are not recommended in women at high risk of gonococcal PID.

225
Q

what are the complications of PID?

A
  1. Tubo-ovarian abscess
  2. Fitz-hugh- curtis syndrome
  3. recurrent PID
  4. ectopic pregnancy
  5. subfertility from tubal blockage
226
Q

what is an ectopic pregnancy?

A

fertilised ovum implants outside the uterine cavity

227
Q

what are the risk factors for ectopic pregnancies?

A

damage to the fallopian tube

previous ectopic pregnancy

history of infertility

smoking

endometriosis

IVF

maternal age over 35

POP and IUCD

228
Q

what are the main sites of ectopic pregnancies?

A

ampulla - most common site

narrow inextensible isthmus

ovary

cervix

caesarean section scar

229
Q

what are the main complications of ectopic pregnancies?

A

Tubal rupture - may lead to maternal death

recurrent ectopic pregnancy

grief, anxiety or depression

230
Q

what are the clinical features of ectopic pregnancy?

A

can have no signs or symptoms

symptoms:

abdominal/pelvic pain - pain increases 6-8 weeks into pregnancy in fallopian tubes. can vary in other places.

amenorrhoea

vaginal bleeding

shoulder tip pain - referred pain

signs:

pelvic

adnexal

abdominal tenderness

can have cervical motion tenderness

abdominal distention

shock

231
Q

how do you diagnose ectopic pregnancy?

A
  1. confirm she’s pregnant e.g. hCG via serum in bloods or urine. serum hCG may be used to determine subsequent management in women with pregnancy of unkown location (PUL)
  2. vaginal and speculum examination - they do not rupture ectopic pregnancy

gentle abdominal examination - do not palpate for pelvic mass as this can increase risk of rupture

  1. Transvaginal US is gold standard tool for diagnosing ectopic surgery
  2. transvaginal scans, serial hCG levels and laparoscopy can be used used to distinguish between normal intrauterine pregnancy, ectopic, miscarriage and a molar pregnancy
  3. serum progesterone can be used to evaluate pregnancy visibility
232
Q

how do you manage ectopic pregnancy?

A

depends on numerous factors:

  1. is she haemodynamically stable? - are her vital signs normal?
  2. site of implantation of ectopic pregnancy
  3. risk of tubal rupture
  4. serum hcG level see if its doubling every 2 days which is typical in normal pregnancies.
  5. woman needs to understand the diagnosis and risk of ectopic pregnancies

Expectant management - expects to be resolved naturally. no active management required

option for a few women: PUL, minimal or no symptoms and are clinically stable.

hcG should ideally be falling <1500 check every 48hrs until confirmed fall, then weekly when <15 IU

medical management:

methotrexate - kills ectopic

must have insignificant pain, unruptured ectopic pregnancy with an adnexal mass smaller than 35 mm with no visible heartbeat

hCG level less than 1500 IU/L

surgery:

salpingectomy or salpingotomy - performed laparoscopically or by open surgery

first line for women unable to return for follow up after methotrexate treatment or have the following:

significant pain

adnexal mass of 35 mm or larger

fetal heartbeat visible on US scan

serum of hCG level of 5000 IU/L or more

233
Q

what is a pregnancy of unknown location (PUL)?

A

there is no sign intrauterine or ectopic pregnancy or retained products of conception in the presence of a positive pregnancy test or serum hCG >5 IU

234
Q

what is a miscarriage?

A

the spontaneous loss of a pregnancy before 24 weeks of gestation

early miscarriage - occurs before 13 weeks of gestation

late miscarriage - occurs between 13 and 24 weeks of gestation

235
Q

what is a complete miscarriage?

A

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

236
Q

what is an incomplete miscarriage?

A

diagnosed non viable pregnancy in which bleeding has begun but pregnancy tissue remains in the uterus

237
Q

what is a missed miscarriage?

A

aka delayed or silent miscarriage

diagnosed with a non viable pregnancy is identified on US without bleeding or pain

238
Q

what is a threatened miscarriage?

A

diagnosed when there is vaginal bleeding in the presence of a viable pregnancy in the first 24 weeks of gestation

239
Q

what is an inevitable miscarriage?

A

diagnosed non viable pregnancy in which bleeding has begun and the cervical OS is open, but pregnancy tissue remains in the uterus. The pregnancy will proceed to incomplete or complete miscarriage

240
Q

what are the causes of miscarriage?

A

chromosomal abnormalities - most common cause of first trimester

defects in development of the placenta or embryo

  1. recurrent miscarriages

no cause of recurrent miscarriage can be determined in 1/2 of couples

endocrine cause

infective cause

genetic abnormalities

241
Q

what are risk factors for miscarriages?

A

maternal age

number of previous miscarriages

occupational and environmental factors - heavy metals, pesiticide, high dose radiation

lifestyle factors - stress, smoking and obesity

242
Q

what are the symptoms of miscarriages?

A

symptoms of pregnancy (amenorrhea, breast tenderness) and vaginal bleeding in first 24 weeks of pregnancy ( brownish discharge to bright red bleeding)

can also get lower abdominal cramping pain or lower backache

243
Q

how do you diagnose miscarriage?

A

look for symptoms of ectopic pregnancy

confirm pregnancy with a urine pregnancy test

244
Q

what reproductive signs suggest a patient might have turner’s syndrome?

A

raised FSH/LH in primary amenorrhoea

245
Q

what is premature ovarian failure

A

transient or permanent loss of ovarian function before the age of 40

FSH raised

characterised by menstrual disturbance e.g. amenorrhoea or oligomenorrhoea

246
Q

what pain relief can you give in labour?

A

Pharmacological

  1. Entonox - 50% nitrous oxide, 50% air - used in early labour
  2. Opiates:

pethididne or diamorphine

Mum SE: nausea and vomiting
Foetal SE: drowsy, neonatal respiratory distress

  1. Epidural

It is the most effective form of analgesia

disadvantages: slows second stage of labour , increases risk of operational vaginal delivery (not c section tho)

must check BP and IV

SE: causes hypotension for mum can lead to bradycardia for foetus

mum can’t lie flat either as this will increase aortocaval compression

4.Spinal

it is anaethetic of choice for c sections

SE: similar to epidural

  1. Pudendal nerve block

need to push sacrospinous ligament to inject pudendal nerve

commonly used during operative vaginal delivery

247
Q

what is the puerperium?

A

period of recovery and repair following delivery

typically lasts 6 weeks and is associated with return of tissues to pre pregnant state

248
Q

when is the risk of VTE highest during pregnancy?

A

puerperium

249
Q

what is the commonest cause of puerperal pyrexia

A

endometritis

250
Q

what is an operative vaginal delivery?

A

use of an instrument to aid delivery

251
Q

what are the indications for operative vaginal delivery?

A

Maternal:

prolonged 2nd stage

exhaustion

medical avoidance of pushing e.g. severe cardiac disease

Fetal:

suspected fetal distress

for the after-coming head in a breech delivery

252
Q

What is the safety criteria for operative vaginal delivery?

A
  1. consent for procedure
  2. 1/5th or less head palpable per abdomen
  3. membranes have ruptured + fully dilated cervix
  4. exact position of head is known and no maternal tissues are caught before applying instrument
253
Q

what type of forceps are there for operative vaginal delivery?

A

low cavity forceps- are used for ‘lift out’ deliveries when head is on the perineum

Mid cavity non rotational forceps - have a long shank, cephalic and pelvic curves and must only be used when the sagittal suture lies in the AP diameter

mid cavity rotational forceps - have a reduced pelvic curve

254
Q

what is a ventouse (vacuum extraction)?

A

suction devise to suck fetal scalp tissues into a ventouse cup.

baby must be >34 weeks gestation and no maternal coagulopathy

less successful than forceps

kiwi omnicup - most common type of ventouse

255
Q

what are the complications of forceps?

A
  1. perineal trauma
  2. facial bruising
  3. temporal facial nerve palsy
256
Q

what are the complications of ventouse?

A

higher failure rate

cone head - chignon

257
Q

when do you abandon operative vaginal delivery?

A

No descent with each subsequent pull

delivery not imminent after 3 pulls when instrument is correctly applied

proceeding to emergency LSCS

258
Q

what is a caesarean section (C section)?

A

delivery of a foetus through an incision in the abdominal wall and uterus

259
Q

what are the 4 main categories of c section

A

1: immediate threat to life of woman or baby
2: no immediate threat to life or baby
3: requires early delivery
4: delivery at a time that suits the woman and maternal services

260
Q

what are the indications for caesarean sections

A
  1. repeat Cs
  2. fetal compromise such as fetal bradycardia
  3. failure to progress in labour
  4. malpresentation
  5. placenta praevia
261
Q

what types of caesarean sections are there?

A

Lower uterine segment incision: straight incision 3 cm above symphysis pubis with blunt dissection thereafter is recommended

  1. Classical Cs- vertical incision on uterus with either transverse or vertical skin incision

classical rarely used

indications for classical:

very premature fetus

fetus lies transverse with ruptured membranes

262
Q

what are the complications of Cs?

A

intra operative:

haemorrhage

hysterectomy

damage to surrounding organs such as bladder and bowel

post -operative:

VTE

infection

delayed recovery and longer stay in hospital

263
Q

What is pre labour rupture of membranes?

A

any situation in which there is a rupture of membranes before 37 weeks gestation

264
Q

what are the causes of pre labour rupture of membranes?

A

Lower genital tract infection

265
Q

how do you manage pre labour rupture of membranes?

A

sterile speculum exam performed (look for pooling of amniotic fluid ) but avoid digital exam

if negative than do USS for oligohydroaminos

if pre term steroids given antenatally

active management: induce labour

oral erythromycin for 10 days

266
Q

what would the failure to progress in first stage of labour be classed as?

A

longer than 3-8 hour to get to 4cm dilated

267
Q

what is primary arrest?

A

poor progress in active phase of stage 1 with this is being defined as <2cm dilation after 4 hrs

268
Q

what is secondary arrest?

A

poor progress of labour after reaching 7cm dilation

269
Q

what is failure in second stage classed as?

A

with epidural:

primiparous - describing a woman who has been pregnant and given birth once (>3 hrs)

multiparous - >2 hrs

without epidural

primiparous >2 hrs

multiparous >1 hours

270
Q

what are the causes of failure to progress?

A
  1. weak irregular contractions

2. cephalo- pelvic disproportion - disproportion between the foetal head and maternal pelvis

271
Q

how do you manage failure to progress?

A

determine the reason for failure to progress

management employed will depend on exact cause:

1.poor contractions

examine every 2 hours

offer artificial rupture of membranes, if spontaneous hasn’t occurred - vaginal prostaglandins

commence CTG and syntocinin infusion

  1. malposition

usually operative vaginal, depending on how far the baby has descended

can’t perform an operative vaginal if the head isn’t at station yet

272
Q

what is fetal distress?

A

compromise of the fetus due to inadequate oxygen or nutrient supply.

indicates fetal hypoxia

273
Q

what are the causes of fetal distress?

A

uteroplacental insufficiency

274
Q

what are the risk factors of fetal distress?

A

Stillbirth.

Intrauterine growth restriction (IUGR).

Oligohydramnios or polyhydramnios.

Multiple pregnancy.

Rhesus sensitisation.

Hypertension.

Obesity.

Smoking.

Diabetes and other chronic diseases.

Pre-eclampsia or pregnancy-induced hypertension.

Decreased fetal movements.

Recurrent antepartum haemorrhage.

Post-term pregnancy.

275
Q

what are the clinical features of fetal distress?

A

decreased fetal movements

muconeum stained - thick, green and due to baby passing bowel movement

CTG: shows the fetal heart rate response to fetal movement and to maternal contractions

commence CTG if:

maternal request

meconium stained liquor

abnormal heart rate on intermittent auscultation

Augmentation of labour with syntocinin

reduced foetal movements felt

results on CTG which suggest fetal distress:

bradycardia, loss of variability, late deceleration. (do foetal sampling)

276
Q

How do you manage fetal distress?

A

Sit mother up

IV fluids

stop syntoconin

Take fetal blood sample

can give terbutaline and plan for operative delivery

Fetal blood sample- taken from scalp

pH >7.25 is normal

pH 7.-7.25

pH <7.25 - acidotic - immediate delivery required

277
Q

what is a cord prolapse?

A

hen an unborn baby’s umbilical cord slips through the cervix and into the vagina after a mother’s water breaks and before the baby descends into the birth canal.

It is an emergency because cord compression and vasospasm from exposure of the cord causes foetal asphyxia

278
Q

what are the risk factors of cord prolapse?

A

prematurity

polyhydraminos

multiple pregnancies

congenital abnormalities

279
Q

what are the clinical features of cord prolapse?

A

fetal distress following rupture of membranes

pulsatile mass seen on vaginal examination

cord descends ahead of the foetus

if untouched will lead to foetal asphyxia (death)

280
Q

how do you manage cord prolapse?

A

cord prolapse is an obstetric emergency

the presenting part of the fetus may be pushed back into the uterus to avoid compression

if the cord is past the level of the introitus, there should be minimal handling and it should be kept warm and moist to avoid vasospasm

the patient is asked to go on ‘all fours’ until preparations for an immediate caesarian section
the left lateral position is an alternative

tocolytics may be used to reduce uterine contractions

retrofilling the bladder with 500-700ml of saline may be helpful

281
Q

what is shoulder dystocia?

A

a delivery requiring additional obstetric manoeuvres as the shoulders get stuck and are unable to be delivered following delivery of the head

282
Q

what are the risk factors of the shoulder dystocia?

A

macrosomia - a newborn with an excessive birth weight

postdate delivery

increased maternal BMI

poorly controlled diabetes

assisted vaginal delivery

283
Q

how do you manage shoulder dystocia?

A

can die from asphyxia

  1. HELP - get it
  2. McRoberts position and manoeuvre (hyperflexed lithotomy) position:

lie the bed flat and flex mother legs so that thighs are against the abdomen

once in position delivery might occur on its own, but if not apply strong suprapubic pressure

284
Q

what are the complications of shoulder dystocia?

A

fetal asphyxiation and detah

3rd or 4th perineal tears

post-partum haemorrhage

brachial plexus injury:

Erb Palsy (C5,6,7) arm is internally rotated with extension of the forearm and wrist with numbness down the lateral aspect of the arm

Klumpkes palsy (C8-T1): loss of all function of the muscles of the hand, clawing of the fingers

285
Q

what is the pathophysiology amniotic fluid embolism?

A

usually occurs in the later stages of labour, has a high mortality rate

unknown reasons, when amniotic fluid enters the maternal circulation it triggers:

cardiopulmonary compromise

severe disseminated intravascular coagulation

286
Q

what are the risk factors of amniotic fluid embolism?

A

multiple pregnancy

maternal age >35 years

Cs

instrumental delivery

eclampsia

287
Q

what are the clinical features of amniotic fluid embolism?

A

Dyspnoea

chest pain

hypotension

fetal distress

seizures

reduced conscious level

cardiac arrest

feeling cold

majority of women get Disseminated intravascular coagulation (DIC)

288
Q

how do you manage amniotic fluid embolism?

A

supportive care in ITU

majority of women die if they get this. most happen in the first hour

289
Q

what are the clinical features of uterine rupture?

A

most common in VBAC (vaginal birth after cesarean)

will be associated with loss of engagement, fetal distress and maternal shock

290
Q

how do you manage uterine rupture?

A

emergency laparotomy

get the baby out asap!!!!

291
Q

what are the 4 classes of tears in labour?

A

1st degree - injury to perineal skin only

2nd degree - injury to perineal muscle and skin

3rd degree - injury to the perineal muscle, skin and anal sphincter

4th degree - injury to the perineal muscle, skin and anal sphincters and rectal mucosa

292
Q

how do you manage tears in labour?

A

analgesia: pudendal nerve block of no epidural

1-3 degree - stitch up

4th degree - requires repair under GA by a surgeon

293
Q

what are the complications of tears in labour?

A

Urinary incontinence

pelvic organ prolapse

fecal incontinence - if 3rd or 4th degree

294
Q

what is an episiotomy?

A

surgical postero-lateral incision through the skin and perineal muscles that is made from the vagina to the ischio-anal fossa

295
Q

why is an epiostomy carried out?

A

widen the birth canal

reduce the risk of 3rd and 4th tears

296
Q

how do you manage episiostomy?

A

should be stitched up after delivery

women should be given:

laxative

antibioitcs

sufficient analgesia

297
Q

what is the normal term for pregnancy?

A

delivery from 37-42 +0 weeks

298
Q

what is classed as a post term pregnancy?

A

delivery after 42 completed weeks

299
Q

what is classed as pre term pregnancy?

A

moderate to late - 32-37 weeks

very - 28-31 + 6 weeks

extremely - before 28 weeks

300
Q

what are the risk factors of pre term labours?

A

IVF UGR

acute illness: UTI, chest infection

multiple pregnancies

uterine abnormalities

maternal disease: hypertension, diabetes

301
Q

what are the causes of pre term labour?

A

uterine infection

cervical insufficiency

preterm prelabour rupture of membranes

302
Q

how do you manage preterm labour?

A

1.assess risk of delivery:

majority of women who present with threatened preterm labour do not delivery

involves carrying out a fetal fibronectin test

  1. if preterm prelabour rupture of membranes:

cover with antibiotics (erythromycin)

  1. deliberate delaying of delivery

give nifedipine

surgery - cervical closure with Mcdonald suture

  1. preparing for delivery of premature baby

continue fetal monitoring

dexamethasone - 2 doses, 12 hours apart - helps to promote maturity of the lungs by stimulating surfactant production

magnesium sulphate :

given in established labour

given to provide baby with neuroprotection

give calcium gluconate for magnesium sulphate induced respiratory depression

303
Q

what is placental retention

A

a placenta which has not been completely passed

within 30 minute of active management of 3rd stage

within 60 minutes of active management of 3rd stage

304
Q

what are the causes of placental retention

A

pre term delivery

induced labour

maternal age >35

parity >5

placenta accreta:

condition which the placenta embeds into the myometrium due to defective decidua basalis (bottom layer of placenta)

305
Q

how do you manage placental retention?

A

active management of 3rd stage:

Injection of oxytocin and cord is clamped and cut between 1 and 5 minutes after the birth

The placenta is pulled out by the midwife once it has separated from the wall of the uterus

if this doesn’t work:

manual evacuation under anaesthesia - place mother lithotomy position

managing placenta accreta:

section +/- hysterectomy

post-delivery contraception

306
Q

what are the definitions of post- partum haemorrhage?

A

defined as blood loss of > 500mls and may be primary or secondary

primary occurs within 24 hrs

secondary occurs within 24 hrs -12 weeks after delivery

307
Q

what are the risk factors for post-partum haemorrhage?

A

previous PPH

prolonged labour

pre-eclampsia

increased maternal age

polyhydramnios

emergency Caesarean section

placenta praevia, placenta accreta

macrosomia

ritodrine (a beta-2 adrenergic receptor agonist used for tocolysis)

308
Q

what are the causes of post-partum haemorrhage?

A

4 T’s

Tone - uterine atony (uterus lacks tone so won’t contract) - most common (90%)

Trauma - perineal damage, rarely uterine rupture

Tissue - retained placenta (placenta accreta)

Thrombin - DIC (Disseminated intravascular coagulation) due to eclampsia, shock, amniotic fluid or abruption

309
Q

compare the different causes of PPH and the condition of the uterus and different clinical features.

A

main examples:

Uterine atony (most common cause) - vaginal bleeding after the placenta has passed - soft uterus

uterine rupture - severe abdominal pain, vaginal bleeding - painful uterus on palpation

retained placenta - vaginal bleeding with incomplete passage of the placenta - soft or contracted uterus

310
Q

how do you manage PPH?

A

1.ABCDE:

cross match - 4 litres

including two peripheral cannulae, 14 gauge

bimanual uterine massage

IV syntocinon (oxytocin) 10 units or IV ergometrine 500 micrograms

IM carboprost

fluid resuscitation ( 3 litres)

medical option fails:

to control the bleeding then surgical options will need to be urgently considered

intrauterine balloon tamponade is an appropriate first-line ‘surgical’ intervention

other options include: B-Lynch suture, ligation of the uterine arteries or internal iliac arteries

if severe, uncontrolled haemorrhage then a hysterectomy is sometimes performed as a life-saving procedure

311
Q

what blood tests can you carry out for fetal anomaly

A

Combined tests:

main choice

uses NT + free hCG + pregnancy associated plasma protein (PAPP-A) + woman’s age

achieves high detection rate for:

Down’s syndrome(Tri 21) - learning disabilities, characteristic appearance, cardiac abnormalities

Edwards syndrome (Tri 18) - small chin, low set ears, rocker bottom feet

Patau syndrome (Tri 13) - microcephaly, holoprosencephaly, exomphalos and cleft lip

intergrated test:

better than combined but too expensive

uses NT+ PAPP-A in the 1st trim + quadruple test

Quadruple test:

blood test at 16 weeks using a dating scan plus alpha fetoprotein

312
Q

what would down’s syndrome levels be with the following:

hCG

Inhibin A

AFP

PAPPA

estriol

A

high:

hCG, Inhibin A

low:

PAPPA

AFP

Estriol

313
Q

would twins have a high AFP levels or low levels?

A

High

314
Q

when is genetic testing offered?

A

family history of genetic condition

downs screen comes back high risk

315
Q

name two types of invasive testing and reasons for their advantages.

A
  1. Chorionic villus sampling
    US guided sampling of the placenta

taken 10-13 weeks

advantages: allows earliest diagnosis of chromosomal abnormality
2. Amniocentesis

aspiration of fluid containing fetal cell from skin and gut

16 weeks onwards

best for downs

advantages:
diagnose fetal infections such as CMV

safer as miscarriage is lower

316
Q

what genetic tests can you carry out?

A

targeted gene - FISH

whole genome - array CGH

317
Q

what are the two types of intra uterine growth restriction (IUGR)?

A
  1. symmetrical - head and abdominal cirrcumference is small - suggest baby has grown less well than expected throughout pregnancy
  2. asymmetrical - head circumference is normal but abdominal circumference is small. suggests reduction in has occurred in later pregnancy - due to placental insufficiency
  3. asymmetrical -
318
Q

what is intra uterine growth reduction?

A

corrected birth weight is less than the 10th centile

319
Q

what are the clinical features of IUGR?

A

smaller than expected fundal height

reduced fetal movements

320
Q

what are the causes of IUGR?

A

1.Maternal related

lack of nutrition

lifestyle: alcohol

beta blockers

2.fetal related:

multiple pregnancies

congenital

3.Utero placental related

pre eclampsia

placental insufficiency

321
Q

what are the complications of IUGR?

A

still birth

pre term labour

322
Q

how do you manage IUGR?

A

serial growth charts

increase monitoring

address modifiable risk factors

323
Q

what is large for date foetus?

A

symphysial fundal height > 2cm than expected for date

324
Q

what are the causes of large for date foetus?

A

diabetes

polyhydramnios

multiple pregnancies

constitutionally large

325
Q

what types of twins are there based on zygosity.

A

dizygotic twins: 2 cells

will be dichorionic and diamniotic (non identical twins) - 2 separate placentas, 2 separate amniotic sacs

monozygotic twins:

  1. diachronic diamniotic -2 separate placentas, 2 separate amniotic sacs
  2. monochorionic diamniotic - most common - 1 placenta 2 sacs
  3. monochorionic monoamniotic - 1 sac ,1 placenta (rarest)
326
Q

what is polyhydramnios?

A

excessive amount of amniotic fluid (>1500 ml, >8cm)

327
Q

what are the main causes of polyhydraminos?

A

twins

diabetes

hydrops fetalis

328
Q

what are the clinical features of polyhydraminos?

A

SOB

abdominal discomfort

feels like she is going to ‘burst’

329
Q

what are the complication of polyhydraminos?

A

preterm labour

cord prolapse

premature rupture of membranes

330
Q

how do you manage polyhydraminos?

A

address and treat modifiable risk causes

US to confirm diagnosis and asses fetal wellbeing

increase monitoring throughout pregnancy

331
Q

what is oligohydraminos?

A

inadequate amount of amniotic fluid (<500 ml at 32-36 weeks)

332
Q

what are the causesoligohydraminos?

A

IUGR

Renal ageneiss

preclampsia

333
Q

how do you manage oligohydramnios?

A

address and treat modifiable risk causes

US to confirm diagnosis and asses fetal wellbeing

increase monitoring throughout pregnancy

334
Q

what is potters syndrome?

A

characteristic changes in foetuses due to oligohydramnios

club feet

pulmonary hypoplasia

potters sequence - flat nose, recessed chin, low set ears

335
Q

what is rhesus haemolytic disease?

A

When a mother is Rh negative (no antigen expressed) and the baby is Rh positive (antign expressed)

Rhesus antigen is an antigen on red blood cells

IgM is produced first and DOESN’T cross the Placenta first pregnancy is not affected

IgG will eventually be produced and DOES cross the placenta and will damage any future pregnancies by breaking down any fetal RBC

will lead to:

progressive anaemia

cardiac failure

hepato-splenomegaly

fetal death

336
Q

how do you prevent rhesus haemolytic disease?

A

anti D at 28 and 34 weeks to negative mothers

337
Q

how do you diagnose rhesus haemolytic disease?

A

kleihauer: positive if fetal and maternal blood has mixed. also used to test if enough anti D has been given

indirect coombs: tells you whether the mum is sensitised or not

positive - sensitised
negative - not

Anti D cannot be used if mother is coombs positive

anti D only given if:

mother Rh negative

Baby Rh positive

mother is coombs negative

338
Q

how do you manage of fetus with rhesus haemolytic disease?

A

depend on the severity of disease and the gestation

if still viable:

fetal blood transfusion

delivery if appropriate gestation

assess well being via US

339
Q

what effect do teratogenic drugs have on babies?

A

1st trimester

impacts foetal organ development

2nd and 3rd

will affect growth and can cause intellectual/ behavioural abnormalities

340
Q

when can folic acid and multivitamins be taken in pregnancy?

A

3 months pre conception

duration of first trimester

341
Q

Which vitamin will need supplementation during pregnancy?

A

D

342
Q

give examples of teratogenic drugs?

A

ACE I/ARB

Androgens

Lithium- cardiac abnormalities

retinoid - used in abortion - causes ear cardiac and skeletal defects

warfarin

343
Q

what drugs are safe in pregnancy?

A

Heparin

methyldopa

cyclizine

paracetamolantacids

nitrofurantoin

344
Q

what is hyperemesis gravidarum

A

the extreme form of ‘nausea and vomiting of pregnancy’ (NVP)

345
Q

what are the association of hyperemesis graviadum?

A

high hCG levels

Increased placental mass

First pregnancy

History of hyperemesis gravidarum in a previous pregnancy

multiple pregnancy (twins)

H pylori infeciton - nausea and vomiting of pregnancy related

346
Q

when do you refer a patient with nausea and vomiting of pregnancy?

A

Continued nausea and vomiting and is unable to keep down liquids or oral antiemetics

Continued nausea and vomiting with ketonuria and/or weight loss (greater than 5% of body weight), despite treatment with oral antiemetics

A confirmed or suspected comorbidity (for example she is unable to tolerate oral antibiotics for a urinary tract infection)

347
Q

what is the triad of diagnosis for hyperemesis graviadum?

A

5% pre-pregnancy weight loss
dehydration
electrolyte imbalance

348
Q

what are the clinical features of hyperemesis gravidarum?

A

nausea

vomiting

loss of weight

inability to tolerate food and drink

349
Q

how do you diagnose hyperemesis gravidarum?

A

Pregnancy-Unique Quantification of Emesis (PUQE) score can be used to classify the severity of NVP.

FBC,ketones and UTI

raised beta hCG

triad:

5% pre-pregnancy weight loss
dehydration
electrolyte imbalance

350
Q

what are the consequences of hyperemesis gravidarum?

A
Wernicke's encephalopathy
Mallory-Weiss tear
central pontine myelinolysis
acute tubular necrosis
fetal: small for gestational age, pre-term birth
351
Q

how do you manage hyperemesis gravidarum?

A

antihistamines should be used first-line

oral cyclizine or oral promethazine

oral prochlorperazine is an alternative

ondansetron and metoclopramide may be used second-line
metoclopramide may cause extrapyramidal side effects. It should therefore not be used for more than 5 days

ondansetron during the first trimester is associated with a small increased risk of the baby having a cleft lip/palate. if ondanestron is used then these risks should be discussed with the pregnant woman

admission may be needed for IV hydration

352
Q

what happens to blood pressure in normal pregnancy?

A

BP falls in 1st half of pregnancy (up to 24 weeks)

usually increases to pre-pregnancy levels by end

353
Q

what is the definition of hypertension in pregnancy?

A

140 mm Hg- systole

90 mm Hg - diastole

354
Q

what are the 3 categories of hypertension in pregnancy are there?

A
  1. pre existing (chronic) - women who have a history of hypertension before or an elevated BP (>140/90) before 20 weeks gestation
  2. Pregnancy induced hypertension (PIH) - hypertension in the second half of pregnancy
  3. pre-eclampsia - hypertension in association with proteinuria ( >0.3g/24 hrs)
355
Q

compare the clinical features of the different types of hypertension associated with pregnancy?

A

chronic - no proteinuria no oedema, more common with older women.

PIH - no proteinuria, no oedema. Resolves following birth (1 month roughly). they are at risk of developing pre eclampsia or hypertension later in life

Pre eclampsia -Proteinuria, or renal insufficiency ( creatinine 90 micromol/litre), Liver involvement (elevated transaminases) , Neurological complications (eclampsia, altered mental status), Haematological complications ( thrombocytopenia) , Uteroplacental dysfunction (fetal growth restriction)

356
Q

how do you manage hypertension in pregnancy?

A

pre existing:

stop ACE I/ ARB prior to conception

Do not rush to start medication as BP which will naturally decrease in pregnancy

Refer to specialist to increase antenatal care to optimise drug management and to monitor fetal wellbeing

women who are high risk of pre eclampsia:

Ensure that aspirin 75—150 mg daily is prescribed from 12 weeks’ gestation until birth

dip stick for proteinuria or urine protein/creatine ratio to rule out pre eclampsia

Drug medication:

Give anti hypertensives

you can breast feed with all of these

methyldopa

labetolol

Nifedipine SR

Hydralazine

avoid diuretics/ ACE inhibitors

357
Q

what would be classed as a hyperintensive emergency for pregnant women?

A

> 160/110

358
Q

what is pre-eclampsia?

A

emergence of high BP during pregnancy that may be a precursor to developing eclampsia

new onset blood pressure >140/90 mmHg after 20 weeks of pregnancy and 1 or more of the following:

proteinuria

other organ renal involvement - renal insufficiency ( creatinine 90 micromol/litre), Liver involvement (elevated transaminases) , Neurological complications (eclampsia, altered mental status), Haematological complications ( thrombocytopenia) , Uteroplacental dysfunction (fetal growth restriction)

359
Q

what are the risk factors of pre -clampsia?

A

high risk:

previous severe or early onset pre eclampsia

chronic hypertension or hypertension in previous pregnancy

CKD

diabetes mellitus

SLE

moderate risk:

1st pregnancy

> 40 year old

BMI >35 Kg/m2

family history of pre-eclampsia

360
Q

what are the classically features of pre -eclampsia?

A

proteinuria

oedema

new onset hypertension

features of severe pre-eclampsia:

headache

flashing lights

HELLP: haemolysis , elevated LFT, Low platelets

HELLP presents with:

epigastric or RUQ pain

N+V

lethargy

Eclampsia: tonic clonic seizures due to pre-eclampsia

361
Q

how do you diagnose Pre eclampsia?

A

hypertension >140/90 mm Hg and urine PCR >0.3 mg/dL

proteinuria

if absent proteinuria look for:

Thrombocytopenia (platelets <100 x109/l)

serum creatinine >88μmol/L

elevated transaminases

TESTS:

dip stick and pcr for proteinuria

BP - for hypertension

Bloods: FBC ( anaemia and thrombocytopenia) , LFT and coagulation

Fetal wellbeing: US (include umbilical artery dopplers)

362
Q

how do you manage pre-clampsia

A

emergency secondary care assessment for any woman in whom-pre eclampsia is suspected

women with blood pressure >160/110 mmHg will be observed

further management:

oral labetalol first line

give nifedipine if asthmatic

363
Q

what are the effects of pre eclampsia?

A

plasma volume decrease

peripheral erisstance increase

placental ischaemia

364
Q

what are the severe complications of pre- eclampsia?

A

eclampsia

HELLP

cerebral haemorrhage

IUGR

renal failure

placental abruption

365
Q

what is post maturity (prolonged pregnancy)?

A

pregnancy exceeding 42 completed weeks

366
Q

what are the problems associated with postmaturity?

A

intrapartum deaths 4 times more common

early neotnatal deaths 3 times more common

increased rates of induction of labour

placental insufficiency

macrosomia

fetal skull more ossified so less mouldable

increased fetal distress in labour

367
Q

what are the reasons for home birth?

A

woman feels more relaxed at home

fear of hospitals

continuity with a named midwife

368
Q

is maternal mortality effected by home birth?

A

no stays same however perinatal mortality is slightly increased

369
Q

what types of diabetes do pregnant women get?

A

Gestational diabetes - 87% of cases

Type 1 -7% of cases

Type 2- 5% of cases

370
Q

what is gestational diabetes?

A

a condition characterized by an elevated level of glucose in the blood during pregnancy, typically resolving after the birth.

diagnostic criteria

fasting glucose >5.6 mmol/L
or
OGTT glucose >7.8 mmol/L

371
Q

what are the risk factors of gestational diabetes?

A

BMI of >30 Kg/M2

Previous macrosomic baby weighing 4.5 Kg or above

previous gestational diabetes

first degree- relatives with diabetes

family origin with a high prevalence of diabetes (south asian and middle eastern)

372
Q

what is the management of gestational diabetes?

A
  1. refer to joint diabetes and antenatal clinic within a week
  2. teach women taught about self-monitoring of blood glucose
  3. advise about diet
  4. screening for gestational diabetes

fasting glucose >5.6 mmol/L
or
OGTT glucose >7.8 mmol/L -diagnostic test of choice for gestational diabetes

5.if fasting glucose is <7 mmol/l then you can:

trial and diet exercise

if glucose target isn’t reached after 1-2 weeks then give metformin

  1. If fast glucose is >7mmol/l then:

no exercise and diet give insulin straightaway

  1. if fasting glucose is between 6-6.9 mmol/l there is evidence of macrosomia or hydraminos:

offer insulin

  1. give glibenclamide if they can’t tolerate metformin or those who fail to meet the glucose targets with metformin but decline insulin treatment
373
Q

what should pregnant women with previous gestational diabetes should be offered at 24-28 weeks?

A

OGTT -

374
Q

how do you manage pre-existing diabetes?

A

weight loss for women with BMI >27

stop oral hypoglycaemic agents - apart from metformin and commence insulin

folic acid 5mg/day to 12 weeks gestation

anomaly scan at 20 weeks include 4 chamber view of heart

tight glycaemic control

treat retinopathy

375
Q

what effect has hypothyroidism on pregnancy?

A

minimal effect on pregnancy however it is associated with:

infertility

oligomenrrhoea

menorrhagia

increased rate of miscarriage

376
Q

how do you manage hypothyroid?

A

dose of thyroxine may need to increase it (up to 50% as early as 4-6 weeks of pregnancy)

thyroxine is safe in pregnancy and breastfeeding

377
Q

what effect has hyperthyroidism on pregnancy?

A

typically worst in first trimester and then improves in the second and third

378
Q

what are the impacts of hyperthyroidism if untreated?

A

Recurrent miscarriage

preterm delivery

IUGR

379
Q

how do you manage hyperthyroidism in pregnancy?

A

PTU (transient propylthiouracil) or carbimazole. PTU preferred

PTU crosses placenta less and is used in newly diagnosed thyrotoxicosis in pregnancy

380
Q

how do you manage epilepsy in pregnancy?

A

preconcepton:

  1. optimise treatment aim for seizure control on lowest dose - monotherapy
  2. folic acid 5mg for >3 months prior to conception. keep giving until end of 1st trimester

Risks of uncontrolled epilepsy outweigh risks of medication to the foetus:

  1. aim for monotherapy
  2. carbamazepine - often considered the least teratogenic of the older antiepileptics
  3. Phenytoin - associated with cleft lip palate. take vitamin K last month of pregnancy
  4. Iamotrigine - may need to increase dose in pregnancy
  5. sodium valproate - only give if you have to. significant risk f neurodevelopment in children
381
Q

when are pregnant women screened for anaemia?

A

8-10 weeks

28 weeks

382
Q

when would you prescribe oral ferrous sulfate or ferrous fumarate in pregnant women for anaemia?

A

first trimester: <100g/L

2nd/3rd <105 g/L

post partum <100 g/L

383
Q

when is a VTE at its highest risk in pregnant women?

A

puerperium period

384
Q

what are the risk factors for pregnant women in developing a VTE?

A
  1. age
  2. parity >3
  3. c section
  4. pre eclampsia
  5. prolonged labour
  6. OHS
385
Q

what are the clinical features of VTE in pregnant women?

A

DVT - leg swelling (left leg more likely), pain, redness, oedema, tenderness

Pulmonary embolism (PE)- SOB, chest pain, haemoptysis, Raised JVP

386
Q

how do you diagnose VTE?

A

FBC

U&E

LFTs

  1. DVT - doppler US
  2. PE:

1st line: CXR and ECG

2nd: VQ, CTPA

D-DIMER limited use in pregnancy as usually raised anyway

387
Q

how do you manage VTE in pregnancy?

A

warfarin contraindicated

S/C LMWH preferred to IV heparin (less bleeding)

388
Q

when would cholestasis of pregnancy present?

A

3rd trimester

389
Q

what are the clinical features of Cholestasis in pregnancy?

A

intense itch- palms and soles

biochem - raised bilirubin (jaundice)

390
Q

how do you manage cholestasis in pregnancy?

A

ureseodeoxycholic acid fo ritch

regular check of LFT

vitamin K pre and post birth to reduce change of haemorrhagic disease of new born

induction of labour 37-38 weeks in

391
Q

which SSRI can you prescribe in pregnancy?

A

setraline

remember aim for monotherapy at the lowest dose

392
Q

what is parovirus B19?

A

DNA virus spread by respiratory droplets with 4-20 day incubation

393
Q

what are the clinical features of parovirus?

A

child:

slapped cheek rash

maculopapular rash
fever

arthralgia

parents:

50% of adults are asymptomatic.

little consequence on mum if she has it unless she is immunocompromised

394
Q

how do you diagnose parovirus B19?

A

Parvovirus B19-specific immunoglobulin M (IgM)- (PCR) analysis

IgG titres increase - antenatal booking blood samples.

results:

Positive for IgG and negative for IgM - women has past but not recent parovirus - immune

Negative for both IgG and IgM, she is susceptible to infection. repeat blood test if negative again she hasn’t been infected yet.

Positive for IgM and negative for IgG, repeat a blood test immediately

positive IgM suggest recent infection

395
Q

how do you manage parovirus B19 in pregnant women?

A

Serial fetal ultrasound scans and Doppler assessment to detect fetal anaemia, heart failure, and hydrops.

If there is suspected fetal hydrops, options include:

Parvovirus B19 viral DNA detection in amniotic fluid.

Fetal blood sampling and intrauterine red blood cell transfusion, which may reduce the fetal mortality rate.

396
Q

what are the complication of parovirus B19 in foetuses?

A

cardiac failure

fetal hydrops - severe swelling (oedema)

10% of foetus infected at <20 weeks die

397
Q

what is antepartum haemorrhage?

A

vaginal bleeding after 24 weeks prior to delivery of the fetus

398
Q

what are the causes of antepartum haemorrhage?

A

placental abruption

placenta praevia

vasa praevia

lower genital tract causes:

cervical polyps

erosions and carcinoma

vaginitis

399
Q

what history would you ask for with suspected APH?

A
  1. gestation
  2. bleeding

When did it start?

what were you doing when it started?

colour of blood?

how mych lost?

how long did it last?

any clots?

has this happened in other pregnancies?

  1. associated

breaking of water, dizziness?

abdominal pain, vomiting?

urinary frequency?

  1. current pregnancy?

could you feel the baby move before bleed?

any changes in fetal movements?

how has the pregnancy been beside this?

what antenatal appointments have you had?

what did they say in the appointments?

  1. past obstetric

is this your first pregnancy?

when and how did you deliver your last one?

  1. general

blood group?

when was your last smear?

lifestyle - smoking

n.b. ask about domestic abuse as well

400
Q

how do you diagnose and investigate Antepartum haemorrhage?

A

Maternal:

vital signs - look for shock

pregnant abdomen exam

speculum and then PV - only do PV when placenta praevia is ruled out (US)

Fetal: assess for well being

Doppler

CTG

investigations:

FBC, coagulation, Kleihouer (blood test used to measure amount of fetal haemoglobin transferred from a fetus to a mother’s bloodstream)

imaging: Pelvic US either abdominal or transvaginal

401
Q

what is a placental abruption?

A

part of the placenta becomes detached the uterus

outcome depends on the amount of blood loss and degree of separation

402
Q

what is placenta praevia?

A

when the placenta partially or completely implants in the lower segment of the uterus

403
Q

what types of placenta praevia are there?

A

minor: does not reach the internal os (opening of the uterus)
major: either partially or completely covers the os

404
Q

what are the associated factors of placenta praevia?

A

multiparity

multiple pregnancy

embryos more likely to implant on a lower segment scar from previous caesarean section

fibroids

endometriosis

405
Q

what are the clinical features of placenta praevia?

A

shock in proportion to visible loss

no pain

uterus not tender

lie and presentation may be abnormal

fetal heart usually normal

coagulation problems rare

small bleeds before large

406
Q

how do you diagnose placenta praevia?

A

often picked up on 20 weeks abdominal US

Transvaginal US is superior to abdominal US however

Repeat scan at 32 weeks if major praevia

repeat scan at 36 weeks if minor

407
Q

how do you manage placenta praevia?

A

1.if low lying 20 week scan:

Repeat scan at 32 weeks if major praevia

repeat scan at 36 weeks if minor

2.final US:

36 -37 weeks to determine the method of delivery

elective caesarean sections III/IV between 37-38 weeks

if grade I then a trial of vaginal delivery may be offered

known placenta praevia goes into labour prior to the elective CS than emergency should be performed due to risk of post-partum haemorrhage

3.Placenta praevia with bleeding

admit

ABC to stabilise the woman

if not able to stabilise - emergency CS

if in labour or term reached - emergency CS

4.Prognosis:
death is now extremely rare

408
Q

what are the associated factors of placental abruption?

A
  1. Proteinuric hypertension
  2. cocaine
  3. Multiparity
  4. maternal trauma
  5. increasing maternal age
  6. pre eclampsia
  7. DIC
409
Q

what are the clinical features placental abruption?

A
  1. shock out of keeping with visible loss
  2. pain constant
  3. tender, tense uterus
  4. normal lie and presentation
  5. fetal heart: absent/distressed
  6. coagulation problems
410
Q

how do you manage placental abruption?

A

Fetus alive and <36 weeks

  1. fetal distress: immediate caesarean
  2. no fetal distress: observe closely, steroids, no tocolysis, threshold to deliver depends on gestation

Fetal alive >36 weeks

  1. fetal distress: immediate caesarean
  2. no fetal distress: deliver vaginally

fetus dead:

induce vaginal delivery

411
Q

what are the complications of placental abruption?

A

maternal:

Shock

DIC

renal failure

PPH

Fetal:

IUGR

hypoxia

death

412
Q

what is vasa previa?

A

when the fetal blood vessels develop within the membrane

when the membranes rupture the fetal vessels will too resulting in catastrophic bleed and rapid onset of fetal distress and death

413
Q

what are the clinical features of vasa previa?

A

sudden painless vaginal bleeding following rupture of membranes

414
Q

how do you diagnose vasa previa?

A

diagnostic: Pelvic ultrasound

CTG: fetal distress

415
Q

How do you manage Vasa previa?

A

if diagnosed pre labour: plan section before term

if diagnosed ROM: emergency section

416
Q

what is a placenta accreta?

A

attachment of the placenta to the myometrium due to a defective decidua basalis.

As the placenta does not properly separate during labour there is a risk of PPH

417
Q

what 3 types of placenta accreta are there?

A

accreta: chorionic villi attach to myometrium
inceta: chorionic villi invade into the myometrium
percreta: chorionic villi invade through the perimetrium

418
Q

what is the main cause of early onset infection in neonates?

A

Group B streptococcus - benzylpenicillin is antibiotic of choice

419
Q

how do you manage reduced fetal heartbeat by gestation?

A

past 28 weeks

handheld Doppler is first step

if no heart beat detected ultrasound should be offered immediately

if heartbeat detected then use CTG to monitor it for the next 20 minutes

between 24 and 28 weeks gestation

a handheld Doppler should be used to confirm presence of fetal heartbeat.

If below 24 weeks gestation

fetal movements have previously been felt, a handheld Doppler should be used.

If fetal movements have not yet been felt by 24 weeks, onward referral should be made to a maternal fetal medicine unit

420
Q

what immunoglobulins would be raised in a mother recently infected with rubella?

A

IgM

421
Q

what is chicken pox caused by?

A

varicella-zoster virus

422
Q

what is the risk of chicken pox to mothers?

A

greater risk of pneumonitis

423
Q

what is the risk of chicken pox to foetus?

A

can develop Foetal varicella syndrome (FVS)

risk of FVS following maternal varicella exposure is around 1% if occurs before 20 weeks gestation

features of FVS include:

skin scarring

eye defects (microphthalmia)

limb hypoplasia

microcephaly

learning disabilities

424
Q

what is the management of chicken pox exposure in pregnancy?

A
  1. mum should be urgently checked for varicella antibodies - if she is unsure if she has been exposed before
  2. if woman <20 weeks gestation is not immune to varicella she should be given varicella-zoster immunoglobulin (VZIG) as soon as possible
  3. if woman> 20 weeks gestation is not immune to varicella then either VZIG or antivirals (aciclovir or valaciclovir) should be given days 7 to 14 after exposure
425
Q

how do you manage chicken pox in pregnancy?

A

if a pregnant woman develops chickenpox in pregnancy then specialist advice should be sought

oral aciclovir should be given if the pregnant women is ≥ 20 weeks and she presents within 24 hours of onset of the rash

if the woman is < 20 weeks the aciclovir should be ‘considered with caution’

426
Q

what is Twin to twin transfusion syndrome (TTTS)

A

two fetuses share a single placenta, meaning that blood can flow between the twins. In TTTS, one fetus, the ‘donor’ receives a lesser share of the placenta’s blood flow than the other twin, the ‘recipient

donor - become anaemic

recipient - fluid overloaded

severe cases can be fatal to one or both

427
Q

when do you scan for TTTS in twins?

A

thus ultrasound examinations performed between 16 and 24 weeks focus on detecting this condition.

428
Q

what do you scan for after 24 weeks in twins?

A

fetal growth restriction.

429
Q

Which additional measure can aid the effectiveness of McRoberts manoeuvre?

A

suprapubic pressure.

430
Q

what are the clinical features of baby blues?

A

Mothers are characteristically anxious, tearful and irritable

431
Q

what are the clinical features of postpartum depression?

A

depression seen in other circumstances

432
Q

what are the clinical features?

A

severe swings in mood (similar to bipolar disorder) and disordered perception (e.g. auditory hallucinations)

433
Q

what would a bishop score <5 mean?

A

labour is unlikely to start without induction

434
Q

what would a bishop score >8 mean?

A

‘favourable’ - a high chance of spontaneous labour, or response to interventions made to induce labour

435
Q

how do you induce labour?

A

vaginal prostaglandin E2 (PGE2) - main choice

Amniotomy with an amnio hook is only appropriate if the cervix is favourable for this intervention (it is ripe and slightly dilated) can give oxytocin along with it.

436
Q

what is a molar pregnancy (Hydatidiform mole)?

A

pre-cancerous form of gestational trophoblastic disease.

non viable pregnancies.

clinical features: vaginal bleeding in early pregnancy and a uterus which is large for dates.

Ultrasound: appears as a solid collection of echoes with numerous small anechoic spaces which resembles a bunch of grapes (also known as ‘snow-storm’ appearance).

bloods: High beta hCG, low TSH, high thyroxine

437
Q

when does the uterus extend to the umbilicus?

A

20 weeks

438
Q

what are the indications for antibiotics in problems with breastfeeding?

ii. what would be firstline?

A

infected nipple fissure

symptoms not improving after 12-24 hours despite effective milk removal

and/or breast milk culture positive

ii. flucloxacillin for 10-14 days or erythromycin or clarithromycin if penicillin allergic.

439
Q

what is Post partum Haemorrhage (PPH)?

A

defined as blood loss of > 500mls after giving birth

440
Q

what is the most common cause of PPH?

A

uterine atony

441
Q

how do you manage PPH?

A

ABC including two peripheral cannulae, 14 gauge

IV syntocinon (oxytocin) 10 units or IV ergometrine 500 micrograms

IM carboprost

surgery:

intrauterine balloon tamponade

442
Q

what are the clinical features of vulval carcinoma?

A

lump or ulcer on the labia majora

inguinal lymphadenopathy

may be associated with itching, irritation

443
Q

what is the most effective form of emergency contraception?

A

copper intra-uterine

is 99% effective regardless of where it is used in the cycle

criteria:
inserted within 5 days of UPSI, or if a woman presents after more than 5 days then an IUD may be fitted up to 5 days after the likely ovulation date

444
Q

how do you manage antiphospholipid syndrome in pregnancy?

A

aspirin + LMWH

445
Q

what are the clinical features of hydatidiform mole?

A

vaginal bleeding

uterus greater than expected for gestational age

abnormally high serum hCG

snow storm appearance of mixed echogenicity

446
Q

what is vesicovaginal fistula associated with?

A

continuous dribbling incontinence after prolonged labour

patient from an area with limited obstetric services.

447
Q

what is sheehan’s syndrome?

A

post partum hypopituitarism

reduction in function of pituitary gland due to hypovolaemic shock

features:

hypothyroidism

problems with milk production

amenhorrhea

448
Q

what is RMI index based on?

A

CA 125

menopausal status

US findings

449
Q

Which of the following changes would you expect to see in a healthy pregnant patient as compared to before pregnancy?

Increased serum haemoglobin

Increased serum platelets

Increased serum creatinine

Decreased serum urea

Decreased urine protein

A

decreased serum urea

Normal laboratory findings in pregnancy: Reduced urea, reduced creatinine, increased urinary protein loss

450
Q

During a lower segment Caesarian section, what are the layers in between the skin and the fetus?

A
Superficial fascia
Deep fascia
Anterior rectus sheath
Rectus abdominis muscle (not cut, rather pushed laterally following incision of the linea alba)
Transversalis fascia
Extraperitoneal connective tissue
Peritoneum
Uterus
451
Q

what are causes of nipple discharge?

A
  1. physiological
  2. Galactorrhoea - commonest cause may be response to emotional events
  3. hyperprolactinaemia - commonest type of pituitary tumour
  4. mammary duct ectasia - commonest cause in menopausal women
  5. carcinoma - often blood stained. palpable lump
  6. intraductal papilloma - commoner in younger patients. no palpable lump
452
Q

what can mastitis develop into?

A

a breast abscess

453
Q

how do you manage mastitis?

A

flucloxacillin for 10-14 days. Breastfeeding or expressing should continue during treatment.

454
Q

how do you manage breast abscess?

A

incision and drainage.

455
Q

compare galactocele to breast abscess?

A

galactocele is usually painless, with no local or systemic signs of infection.