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Obs & Gynae > Obs & Gynae > Flashcards

Obs & Gynae Flashcards

1
Q

how does oestrogen act in the follicular phase

A
  • stimulate fallopian tube function
  • thicken endometrium
  • growth and motility of myometrium
  • thin alkaline cervical mucus
  • vaginal changes
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2
Q

how does progesterone act in the luteal phase

A
  • acts on oestrogen-primed cells to cause further thickening of endometrium
  • thickening of myometrium with reduced motility
  • thick acidic cervical mucus
  • changes in mammary tissue
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3
Q

describe the HPG axis at the beginning of the cycle

A
  • follicles part-developed therefore very little steroid or inhibin production
  • low inhibition at hypothal and pituitary therefore fsh and lh levels rise
  • fsh binds to granulosa cells to stimulate development
  • lh acts on theca interna cells to produce oestrogen
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4
Q

describe the HPG axis around the time of ovulation

A
  • rising oestrogen levels causes hpg axis to swtich to positive - increase in oestrogen
  • lh carries on rising
  • fsh rises, but not to same extent due to inhibin production
  • inhibin also means no new follicles can develop
  • lh surge causes ovulation
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5
Q

describe the HPG axis at the end of the cycle

A
  • after ovulation, corpus luteum forms,
  • steroid levels rise - oestrogen + progesterone
  • oestrogen suppresses fsh, progesterone suppresses lh
  • fast drop in hormone and progesterone levels due to lack of fertilisation causes menses
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6
Q

what is the normal range for the ovarian cycle

A

24-32 days

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7
Q

list some of the common causes for menorrhagia

A
  • abnormal clotting: VWF disease, thrombocytopenia, coag disorders, leukaemia etc
  • pathology: fibroids, adenomyosis, endometriosis, polyps etc
  • medical disorders: hypo/hyperthyroid, liver disease, sle, cancer
  • DUB: primary menorrhagia - heavy bleeding with no recognisable pelvic pathology/bleeding disorder
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8
Q

list some of the factors affecting menstrual loss

A
  • age: 4th decade
  • hereditary
  • parity
  • uterina pathology
  • cycle-cycle vaiability
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9
Q

list some of the ways to investigate menorrhagia

A
  • FBC: Hb, platelets, clotting factors as necessary
  • TFTs
  • coagulation
  • USS/TVUS
  • hysteroscopy
  • biopsy
  • (colposcopy)
  • (smear)
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10
Q

list some of the treatments for managing menorrhagia

A
  • progestogens e.g. norethisterone, depot
  • Mefenamic acid/ other NSAIDs
  • tranexamic acid - antifibrinolytic
  • IUCD - Mirena (progesterone-impregnated), not copper coil
  • cocp
  • surgical: endometrial ablation, cold coag treatment, laser; hysterectomy as last result
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11
Q

what is the mechanism of action of tranexamic acid

A

antifibrinolytic - inhibits plasminogen activation into plasmin. plasmin usually causes fibrin degradation - therefore TXA inhibits fibrin breakdown

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12
Q

what is PCOS

A

endocrine disorder of unknown aetiology, which can be hereditary.
accounts for majority of causes of amenorrhoea

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13
Q

what are the pathological features of PCOS

A
  • ovarian hypersecretion of andorgens
  • increased pulsatile secretion of LH
  • ovarian theca cell hyperplasia leading to ovarian enlargement
  • anovulation
  • insulin resistance
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14
Q

what are the clinical features of PCOS

A
  • oligo/amenorrhoea
  • DUB
  • obesity
  • hirsuitism
  • acne
  • ‘string of pearls’ appearance of ovaries on USS
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15
Q

what are the biochemical features of PCOS

A
  • increased LH:FSH ratio
  • decreased sex hormone binding globulin
  • increased free androgen index
  • increased serum insulin
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16
Q

what are the differentials for PCOS

A
  • anovulatory cycles
  • congenital adrenal hyperplasia
  • androgen secreting tumours
  • cushings syndrome
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17
Q

what are the long-term health complications of PCOS

A
  • miscarriage
  • gestational diabetes
  • NIDDM
  • HTN
  • cardiovasc disease
  • endometrial hyperplasia/carcinoma
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18
Q

what is the management for PCOS

A
  • weight loss
  • metformin
  • COCP
  • cyproterone acetate (antiandrogen)
  • ovulation induction in infertility
  • ovarian drilling
  • cyclical progestogen
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19
Q

what is the definition of menopause

A

permanent cessation of menstruation due to loss of ovarian follicular activity - 12 months since LMP

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20
Q

what is LMP

A

last menstrual period - calculated as the first day of the last period a woman has had

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21
Q

what are the symptoms of the menopause

A
  • hot flushes and night sweats
  • irritability, mood changes, lack of concentration, depression
  • reduced libido
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22
Q

what is hrt for

A

oestrogen replacement therapy (combined with progestogens if uterus intact)
used to manage symptoms of menopause

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23
Q

list some of the risks associated with hrt

A
  • effects of unapposed oestrogen: increased endometrial/ovarian/breast cancer risk
  • increased IHD/stroke; adverse effect on lipid profile
  • increased risk of vte; adverse effect on thrombophilia profile
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24
Q

what are the different modes of administration of hrt

A
  • po
  • transdermal
  • implant
  • transvaginal
  • nasal
  • local
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25
Q

what drugs may be given to prevent osteoporosis in postmenopausal women

A
  • bisphosphanates (inhibit osteoclasts)
  • calcium + vit D
  • raloxifene (SERM)
  • exercise
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26
Q

define amenorrhoea

A

primary: no menses by age 14, or no menses by 16 despite presence of secondary sexual characteristics
secondary: previous menstrual cycles, but now without menses for 6 months

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27
Q

list the points in the history that should be asked about when taking an amenorrhoea history

A
  • duration of amenorrhoea
  • contraception
  • vasomotor syndrome
  • galactorrhoea
  • exercise habits
  • stress
  • meds
  • pmhx
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28
Q

list some of the causes of primary amenorrhoea without ssc’s

A
  • constitutional delay
  • GU malformation e.g. imperforate hymen
  • testicular feminisation (XY - female external appearance, but gonads are testes, no ovaries)
  • hyperprolactinaemia e.g. pituitary tumour
  • pregnancy must always be considered
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29
Q

list some of the causes of primary amenorrhoea with ssc’s present

A
  • ovarian failure e.g. chemo, turner syndrome
  • hypothalamic failure e.f. chronic illness, exercise, stress
  • HPG - tumours, head injury, Kallman’s synd etc
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30
Q

list some of the causes of secondary amenorrhoea

A
  • pregnancy
  • PCOS
  • Cushings
  • adrenal/ovarian ca
  • primary ovarian insufficiency
  • hypothalamic amenorrhoea
  • hyperprolactinaemia
  • thyroid disease
  • sheehan’s synd following pregnancy
  • iatrogenic, ‘post pill amenorrhoea’
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31
Q

what would you look for when performing an examination of someone with amenorrhoea

A
  • bmi
  • signs of excessive androgens
  • thyroid disease/cushings
  • ssc’s
  • vaginal/external genital/pelvic examination
  • masses e.g. large ovarian cyst
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32
Q

list some of the investigations you would do on someone presenting with amenorrhoea

A
  • pregnancy test
  • fsh/lh levels
  • prolactin
  • total testosterone/sex hormone-binding globulin
  • tft’s
  • pelvic uss e.g. pcos, anatomy
  • additional: karyotype, mri, ct, hysteroscopy
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33
Q

what is the management of amenorrhoea

A

depends on cause

  • reassure if constitutional
  • structural abnormalities: surgery
  • hrt if premature ovarian failure
  • medical review if prolactin increased due to medicines
  • gh for short stature in turner’s syndrome
  • testicular feminisation - surgical removal of testes
  • fertility clinic referral
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34
Q

list some of the causes of irregular menstrual bleeding

A
  • more common in extremes of age
  • anovulatory cycles
  • pelvic pathology e.g. fibroids, polyps, adenomyosis, ovarian cysts, chronic pelvic infection
  • cancer
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35
Q

what investigations would you perform on a woman presenting with irregular bleeding

A
  • hb level
  • exclude malignancy - smear/hysteroscopy/pipelle(older women especially)/biopsy/colposcopy
  • uss
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36
Q

what is the management for irregular menstrual bleeding

A

if no anatomical defect: Mirena, COCP, progestogens (however these cause withdrawal bleed)
exclude cancer first: pipelle exclusion required in older women before inserting coil

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37
Q

what is the definition of oligomenorrhoea

A

bleeding every 35 days - 6months

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38
Q

what are the hypothalamic reasons for amenorrhoea

A
  • psychological
  • stress
  • low weight/anorexia nervosa
  • excessive exercise
  • tumours
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39
Q

what are the pituitary reasons for amenorrhoea

A
  • hyperprolactinaemia usually due to tumour, or pituitary hyperplasia
  • sheehan’s syndrome
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40
Q

what is the treatment for hyperprolactinaemia

A

bromocriptine - dopoamine agonist

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41
Q

what are the ovarian reasons for amenorrhoea

A
  • pcos
  • premature ovarian failure
  • tumours
  • turners syndrome
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42
Q

what is the general rule in management of post coital bleeding

A

always abnormal except after first intercourse. must always exclude cancer

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43
Q

what is the aetiology of PCB

A

usually due to the cervix not being covered in healthy squamous epithelium - more likely to bleed after trauma

  • ectropions
  • polyps
  • cervical cancer
  • cervicitis and vaginitis
  • atrophic vagina
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44
Q

what is the management of PCB

A
  • check smear history
  • careful inspection of cervix +/- smear
  • ectropions -> cryotherapy freezing
  • polyps -> removed and sent for histology
  • colposcopy to exclude malignant cause
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45
Q

what is the treatment for precocious puberty (<10 y/o or ssc’s before 8)

A

gnrh agonists to inhibit sex hormone secretion if no pathological cause found - helps growth as you dont want the femoral epiphysis to fuse too early
cryproterone acetate to act as anti-androgen

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46
Q

what are the causes of dysmenorrhoea

A

primary or secondary

  • primary: no organic cause found
  • secondary: pathology - fibroids, adenomyosis, endometriosis, PID, ovarian tumours
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47
Q

what is the management of dysmenorrhoea

A
  • if primary: NSAIDs, COCP, reassurance as tends to get better with time
  • if secondary: treat underlying cause if possible, NSAIDs, COCP/POP, GnRH analogues,
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48
Q

what is Premenstrual syndrome and the management for it

A

psychological, behavioural and physical symptoms experienced regularly during luteal phase. often resolve by end of cycle. SSRIs may help, COCP, may do a trial of GnRH analogues

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49
Q

list some of the pathological causes of precocious puberty

A
  • central: increased GnRH due to menigitis, encephalitis, tumours, hydrocepahlus etc
  • ovarian/adrenal: hormone-producing tumours or cysts,
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50
Q

list some of the cases of post menopausal bleeding

A
  • endometrial cancer
  • endometrial hyperplasia +/- atypia
  • polyps
  • cervical cancer
  • cervicitis
  • ovarian cancer
  • cervical polyps
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51
Q

what is the management of PMB

A

all these women should undergo bimanual and speculum examination
TVUS should be performed in all to assess endometrial thickness - if over 5mm, requires hysteroscopy + pipelle or polyp biopsy etc

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52
Q

describe some of the effects that menopause has on the vagina

A

atrophy, urinary symptoms
atrophy can cause dyspareunia, itching, dryness
urinary symptoms can cause urgency, nocturia, frequency, recurrent infection

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53
Q

which hormones may be tested for changes in menopause

A
  • FSH (decreases as oocytes decrease)
  • antimullerian hormone - low levels consistent with ovarian failure as AMH is produced by follicles
  • TFT
  • catecholamines (phaeo)
  • LH, oestrogen, progesterone
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54
Q

list the hromonal and non-hormonal treatments for post-menopausal women

A
  • hrt
  • tibolone: synthetic steroid activated by metabolism
  • andorgens
  • lubricants and moisturisers/oestrogen creams in atrophy
  • bisphosphanates, strontium ranolate, raloxifene, PTH peptides, denusomab, adcal for osteoporosis
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55
Q

what are the benefits of hrt

A

symptom control of flushes, sweats, mood swings etc

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56
Q

what are the risks of hrt

A
  • increased risk of certain cancers

- increased risk of vte

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57
Q

what is the difference between infertility and infundicity

A

infertility - inability for a couple to concieve after one year of unprotected intercourse (6 months for women > 35yo)
infundicity - inability for a couple to produce a live birth

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58
Q

list the categories of causes of infertility

A
  • ovulation defects
  • tubal disease
  • endometriosis
  • uterine factor
  • unexplained
  • male factor
  • other e.g. anovulatory cycles
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59
Q

what is evaluated and males and females in couples who are infertile

A

females: ovary, tubes, corpus, cervix, peritoneum
males: sperm count and function, ejaculate characteristics, anatomic anomalies

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60
Q

what is examined in a female presenting with infertiltiy

A
  • bmi
  • body hair distribution
  • galactorrhoea
  • ssc
  • pelvic abnormalities, fixed/tender uterus
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61
Q

list some of the important points in the history of a female presenting with infertility

A
  • age
  • duration of infertility
  • type of infertility
  • menstrual cycle, ovulation
  • previous surgery, especially pelvic
  • menorrhagia, dysmenorrhoea, pelvic pain
  • PID
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62
Q

list some of the important points in the history of a male presenting with infertility

A
  • general health, diabetes?
  • alcohol intake/smoking
  • previous infections
  • sexual dysfunction - erectile/ejaculatory
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63
Q

list the baseline investigations of a female with infertility

A
  • follicular phase fsh/lh day 2
  • luteal phase day 12 lh/fsh
  • tft, prolactin, testosterone, steroid hormone binding globulin
  • rubella status
  • tests of tubal patency
  • pelvic uss
  • hysteroscopy
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64
Q

what are the different tests for tubal patency

A
  • hysterosalpingography (injection of radioopaque material into uterus)
  • hycosy aka tubal patency test (contrast sonoggraphy - TVUS + contrast)
  • diagnostic laparoscopy + dye (blue dye injected and laparoscopy looks for leakage of dye into abdomen if tubes are patent)
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65
Q

how would you examine a male presenting with infertility

A
  • testicle size
  • testicular position
  • scrotum - varicocoele
  • prostate for chronic infection
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66
Q

what are the tests done for males presenting with infertility

A

semen analysis

- volume, concentration and initial foward motility, morphology

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67
Q

what is the normal volume and conc of sperm in ejaculate

A

> 1.5ml

> 15x10^6/ml

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68
Q

except for semen analysis, what other tests could you perform in a male presenting with infertility

A
  • antisperm antibody
  • fsh/lh/testosterone
  • uss - seminal vesicles, prostate
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69
Q

what is the treatment for anovulation

A
  • clomiphene citrate (SERM) - upgrade hpg axis
  • gonadotrophins/pulsatile lhrh
  • dopamine agonists e.g. bromocriptine in hyperprolactinaemia
  • weight loss/gain
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70
Q

what is the treatment for infertility due to tubal disease

A

surgery

ivf

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71
Q

what is the treatment for male factor infertility

A 
ivi
ivf
intracytoplasmic sperm injection
donor insemination
donor sperm
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72
Q

what is endometriosis

A

condition where there is tissue resembling the endometrium lying outside the endometrial cavity - predominantly in pelvis
these respond to cyclical hormone changes and bleeds at menstruation

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73
Q

what is adenomyosis

A

presence of endometrial tissue within the myometrium

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74
Q

how is adenomyosis diagnosed

A

biopsy

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75
Q

what may be some of the signs found on examination of a patient with endometriosis, if any

A
  • fixed uterus
  • uterine/ovarian enlargement
  • uterine fornix tender
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76
Q

what are the difference ways in which endometriosis presents

A

secondary dysmenorrhoea
heavy periods
dyspareunia
lower abdo pain
epistaxis/rectal bleeding (tissue in extra-pelvic places)
infertility can be found alongside endometriosis

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77
Q

how is endometriosis diagnosed/investigated

A

laparoscopy + biopsy gives diagnosis

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78
Q

what signs are present with endometriosis on laparoscopy

A

if active - powder burn spots and chocolate cysts

scars if inactive; peritoneal defects

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79
Q

what is the management of endometriosis

A 
mefenamic acid
tranexamic acid
cocp
continuous progesterone therapy
gnrh analogues +/- hrt
surgical - lap, diathermy, tah + bso (hysterectomy), removal of adhesions
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80
Q

what happens to endometriosis with pregnancy/menopause

A

regress

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81
Q

what are the symptoms of endometriosis

A 
often asymptomatic
chronic pelvic pain, usually cyclical
dysmenorrhoea
deep dyspareunia
subfertility
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82
Q

list some of the differentials of endometriosis

A
  • adenomyosis
  • chronic pelvic inflammatory disease
  • chronic pelvic pain
  • other pelvic masses
  • ibs
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83
Q

what are the side effects of progestogens

A

fluid retention, weight gain, erratic bleeding, pms

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84
Q

how to gnrh analogues work

A

induce a temporary menopausal state - overstimulation of the pituitary gland leads to down-regulation of gnrh receptors

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85
Q

why is treatment with gnrh analogues limited only to 6 months

A

reversible bone demineralisation occurs

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86
Q

define chronic pelvic pain

A

intermittent or constant pain in lower abdomen or pelvis for at least 6 months’ duration, not occuring exclusively with menstruation or intercourse

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87
Q

list some of the investigations that may be performed in chronic pelvic pain

A

TVUS
MRI
Laparoscopy
ca125?

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88
Q

list some of the possible causes of chronic pelvic pain

A 
endometriosis
adenomyosis
malignancy
ibs
intermittent cystitis
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89
Q

list four common causes of anovulation

A

1) pcos
2) hypothalamic hypogonadism
3) hyperprolactinaemia
4) thyroid disease

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90
Q

at which steps can fertilisation fail

A
  • ovaries: anovulation
  • sperm release: inadequate
  • reaching egg: path may be blocked
  • implantation: may fail
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91
Q

what is the treatment of pcos

A
  • advice on diet and exercise
  • cocp to regulate menstruation and treat hiruitism
  • metformin to increase peripheral sensitivity to insulin
  • clomiphene - antioestrogen to reduce negative feedback ad increase lh/fsh
  • lapaorscopic ovarian diathermy
  • gonadotrophins (lh and fsh) if clomiphene has failed
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92
Q

describe the pathological processes in the hypothalamus that can cause anovulation

A

reduced GnRH release
usually with anorexia nervosa, extreme diet/exercise stress
kallman’s syndrome -> GnRH-secreting hormones fail to develop

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93
Q

how may hypothalamic anovulation be managed

A

weight gain, reducing stressor factors
exogenous gonadotrophins
gnrh pump
bone protection if gnrh low

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94
Q

describe the pathological processes in pituitary causes of anovulation

A

increased prolactin causes decreased GnRH release
usually due to adenomas or hyperplasia of pituitary gland
also can be due to trauma, sheehan’s syndrome after pregnancy

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95
Q

what are the other possible symptoms of anovulation due to pituitary cause (increased prolactin)

A 
amenorrhoea
galactorrhoea
headaches
bitemporal hemionopia
increased prolactin levels on biochem
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96
Q

what is the treatment for hyperprolactinaemia

A

ct to exclude tumour
dopamine agonist e.g. bromocriptine to inhibit prolactin release
surgery

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97
Q

what are the options is semen analysis shows mild oligospermia

A

intrauterine insemination

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98
Q

what are the options if semen analysis shows mod-sev oligospermia

A

ivf +/- intracytoplasmic sperm injection

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99
Q

what investigations should be done is semen analysis is azoospermic

A

examine for presence of vas deferens
karyotype: CF
hormones
may try surgical sperm retrieval

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100
Q

what bloods can be performed in males with abnormal sperm analysis

A

serum fsh, lh, prolactin, testosterone, tsh, karyotype, cf blood test
antisperm antibodies

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101
Q

what are the common causes of abnormal/absent sperm release

A
  • idiopathic
  • drug exposure e.g. alcohol, smoking, anabolic steroids, industrial chemicals etc
  • varicocoele, structural abnormalities, obstruction
  • antisperm antibodies
  • genetic
  • hyperprolactinaemia
  • infections
  • kallmann’s syndrome
  • retrograde ejaculation
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102
Q

what is the management of male infertility

A
  • lifestyle chanegs e.g. stopping smoking, reducing alcohol
  • subcut fsh/lh if hypogonadotrophic
  • assisted conception e.g. IUI, IVF, Intracystoplasmic sperm injection, donor sperm, surgical sperm retrieval
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103
Q

what are some of the factors that may make it impossible for sperm to reach egg in order to fertilise it

A
  • sexual problems e.g. psychological
  • cervical problems
  • tubal damage e.g. infection, pid, adhesions from previous surgery etc
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104
Q

what are the indications for assisted conception

A

other methods have failed, or unexplained cause.
male subfertility identified
tubal blockage, endometriosis or genetic factoes

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105
Q

what are the steps in inducing ovulation in patients with pcos

A
  • weight loss/lifestyle changes
  • clomifene
  • if fails add metformin
  • gonadotrophins
  • ovarian diathermy
  • finally if no success - ivf
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106
Q

what are some of the side effects of induction of ovulation

A
  • multiple pregnancy

- ovarian hyperstimulation syndrome where follicles get very large and painful

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107
Q

what is the gestation limit for termination of pregnancy

A

24 weeks, unless foetal abnormality

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108
Q

what are the current medical methods of termination of pregnancy

A 
mifepristone (antiprogestogen)
given with prostacyclin - different types:
- IM suprostone
- PV metenoprost
- PV gemeprost
- PV/PO misoprostol
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109
Q

what is the regimen for medical termination of pregnancy

A

day1: mifepristone
day3: prostaglandins every few hours (depending on which one used)
day14: follow up

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110
Q

what are the contraindications for TOP

A
  • pregnancy 64 days of gestation or over
  • suspected ectopic
  • chronic hepatic/renal failure
  • haemorrhagic disorders
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111
Q

list some of the complications of abortion

A
  • haemorrhage
  • uterine perforation
  • scar dehisence
  • cervical tears
  • failure
  • post abortion sepsis
  • psychological trauma
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112
Q

list the different types of emergency contraception

A 
hormonal - high dose oestrogen/progesterone 2 tablets 12 hours apart
- levonelle
- ellaOne
works within 72 hours of unprotected sex
iud - within 5 days of unprotected sex
- copper
- mirena
- mifepristone iud
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113
Q

what should be ruled out before inserting iud emergency contraception

A

pelvic infection

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114
Q

list some of the “special groups” of patients who may need adjustment to their contraceptive routine - suggest optimal management for each

A

1) adolescents: encourage barrier to prevent sti’s
2) IBD: redcued absorption - patches, injectibles, implants, IUD, vaginal
3) breastfeeding: not effective on its own - progesterone or IUD 4/52 pp. not oestrogen as affects milk production
4) later life: encourage contraception for at least 2 years after LMP

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115
Q

how does the cocp work

A

exert negative feedback on hpg axis to inhibit lh/fsh release and therefore ovulation
also thins the endometrium and thickens cervical mucus

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116
Q

what is the failure rate of cocp

A

0.2/100 woman-years

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117
Q

what changes with each generation of cocp

A

type of progesterone used

each generation may also have a different oestrogen conc used

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118
Q

what are some of the other useful effects of cocp

A

treating acne/hirsuitism
menstrual cycle regulation
managing dysmenorrhoea
ovarian cysts

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119
Q

what are the common se of progestogens

A

depression, bleeding, amenorrhoea, acne, breast discomfort, weight gain, reduced libido

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120
Q

what are the common se of oestrogens

A

nausea, headache, mucus, fluid retention, weight gain, htn, breast tenderness, bleeding

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121
Q

list some of the factors which may affect cocp absorption

A

diarrhoea, vomiting, some PO abx

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122
Q

how would you advise a women who has vomited and is on the pill

A

if vomited within 2 hours, take another pill or follow “missed pill rules”

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123
Q

how would you advise a woman who has diarrhoea and is on the pill

A

follow “missed pill rules” for every day of the illness

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124
Q

how would you advise a woman who is on antibiotics and the pill

A

carry on taking the pill but also use condoms while being treated with antibiotics, for 7 days

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125
Q

how would you advise a woman on the pill who is going for surgery?

A

stop pill for 4 weeks prior surgery and use condoms/other cover in meanwhile

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126
Q

what are the major complications of cocp

A

vte
mi
this is increased by smoking, age, obesity
also: migraines, htn, cervical/endometrial/breast ca

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127
Q

what are the absolute ci’s for cocp

A 
bmi>40
>35 yo
smoking >15/day
hx of vte/mi/cva
thrombophilia
active breast/endometrial/ovarian ca
pregnancy
chronic liver disease
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128
Q

list the benefits of cocp

A

very effective and acceptable
regular, lighter, less painful periods
manages ovarian/breast cysts, fibroids, endometriosis

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129
Q

what is the regimen for the contraceptive patch

A

applied weekly for 3 consecutive weeks then replaced, followed by patch-free week

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130
Q

what is the combined vaginal ring regimen

A

contraception - releases daily dose of hormones to inhibit ovulation. inserted into vagina, worn for 3 weeks and then removed to allow bleed for 7days
new ring then inserted

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131
Q

what is the mechanism of pop

A

make cervical mucus hostile to sperm, may prevent ovulation, maintains thin endometrium to reduce chance of implantation

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132
Q

what should a woman be advised to do if they miss a pop pill

A

take another asap if within 3 hours and condoms used for a following 2 days

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133
Q

is pop contraception affected by broad spec abx

A

no

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134
Q

what is the regimen for depo-provera

A

im every 3/12

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135
Q

why is depo-provera avoided in younger patients

A

reduced bone density risk

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136
Q

what is nexplanon/implant contraception

A

single progestogen-containing rod is inserted into upper arm under LA

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137
Q

what is the failure rate of nexplanon

A

<0.1/100 woman-years

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138
Q

what is in levonelle

A

levonogestrel

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139
Q

what type of drug is the emergency contraceptive ellaOne

A

selective progesterone receptor modulator

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140
Q

what is the failure rate of condoms

A

2-15/100 woman years - similar for male and female condoms

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141
Q

what is the failure rate of diaphragm/cap

A

<5/100 woman years

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142
Q

how are spermicides used

A

in conjunction with barrier methods - jelly/cream/pessary

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143
Q

how do copper iud’s work

A

prevent fertilisation as copper ion is toxic to sperm

also blocks implantation

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144
Q

are copper iud’s recommended in those with heavy periods

A

no -can in fact increase menstrual loss

mirena coil used instead as it is much more useful

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145
Q

how does the mirena coil work

A

is progestogen-containing, and releases small doses locally

changes cervical mucus and endometrium

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146
Q

what are some of the complications of iud use

A
  • pain or cervical shock on insertion
  • expulsion of device
  • movement into abdomen or lodging into endometrium
  • if pregnancy occurs, it is more likely to be ectopic
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147
Q

if a patient cannot feel the strings of her iud, what should you do

A

pelvic uss to look for iud in the uterus

if no present - axr

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148
Q

what are the absolute ci’s to iud

A 
endometrial/cervical ca
undiagnosed pv bleeding
active/recent pelvic infection
current breast ca
pregnancy
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149
Q

what advice should be given to women put on iud

A

check strings after each period

inform doctor if imb, pelvic pain, vaginal dc, feels may be pregnant

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150
Q

describe female sterilisation

A

interruption of fallopian tubes

  • clips to occlude tubes
  • placement of microinserts to expand and cause fibrosis and occlusion of tubes
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151
Q

what is the failure rate of female sterilisation

A

1/200

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152
Q

how would you counsel a woman asking for sterilisation

A

explain surgical risks, that they and their partner must be certain, tat failure risk is 1/200
discuss alternatives
reversal is not always successful and NOT on the NHS

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153
Q

what is the failure rate of vasectomy (ligation and removal of small section of vas deferens)

A

1/2000

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154
Q

how is vasectomy confirmed to have worked

A

azoospermia confirmed by two negative semen analyses

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155
Q

what is the usual histology type of vulval and vaginal cancer

A

squamous cell ca

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156
Q

what are the main causes of vulval and vaginal cancers

A

hpv/chronic skin disease

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157
Q

what are the main treatments for vulval and vaginal cancers

A

surgery, radio, chemo

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158
Q

what is the peak incidence of endometrial cancer

A

64-74 yo

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159
Q

list the risk factors for endometrial cancer

A

1) obesity
2) nulliparity
3) early menarche, late menopause
4) unapposed oestrogen
5) tamoxifen
6) oestrogen-producing tumours
7) diabetes
8) pcos
9) hnpcc

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160
Q

what is the premalignant stage to endometrial cancer

A

endometrial hyperplasia - can be simple, complex, atypical

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161
Q

how is endometrial hyperplasia treated

A

progestogens

surgery

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162
Q

what is type 1 and what is type 2 endometrial cancer

A

type 1: adenocarcinoma

type2: serous, clear cell, carcinosarcoma

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163
Q

what is the treatment for endometrial cancer

A

medical: progestagens PO/IV, Mirena
surgical: TAH + BSO, peritoneal washings, lap/open TAH, pelvic node disection
if advanced: chemo/radio, hormones, palliative

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164
Q

how is endometrial cancer diagnosed

A

hysteroscopy +
sample - pipelle or less commonly d&c
TVUS - useful for PMB

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165
Q

what is the cut off for thickness of the endometrium before it becomes a concern

A

5mm or more

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166
Q

what are the early signs of endometrial cancer

A

abnormal bleeding - imb/irregular

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167
Q

what are the late signs of endometrial cancer

A

pmb, blood stained vaginal dc

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168
Q

list the different cell lines from which endometrial cancer can arise

A
  • surface epithelium
  • stroma
  • germ cells
  • mets/misc
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169
Q

what are the different types of surface epithelium carcinoma

A
  • serous
  • mucinous
  • endometrioid
  • clear cell
  • brenner
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170
Q

what are the different types of germ cell tumours

A
  • choriocarcinoma
  • dysgerminoma
  • teratoma
  • yolk sac
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171
Q

what are the different types of stroma/cord cell tumour

A

granulosa
theca
sertoli-leydig

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172
Q

what are the risk factors for ovarian tumours

A
  • BRCA 1/2
  • hnpcc
  • nulliparity
  • infertility
  • early menarche
  • late menopause
  • unapposed oestrogen
  • hrt
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173
Q

what is the peak age for ovarian cancer

A

70-74

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174
Q

list some of the factors that decrease risk of ovarian cancer

A
  • cocp
  • pregnancy
  • breastfeeding
  • hysterectomy
  • oopherectomy
  • sterilisation
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175
Q

list the stages of ovarian cancer

A

1) limited to ovary/ies
2) spread to pelvic organs
3) spread to rest of peritoneal cavity
4) distant mets/liver parenchyma/lung

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176
Q

how may ovarian cancer present, if symptomatic

A 
abdo swelling
pain
anorexia, n&amp;v, weight loss
vaginal bleeding
changes in bowel habit
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177
Q

what are the diagnostic investigations for ovarian cancer

A 
pelvic examination
fbc/U&amp;E/LFT
CA125
transvaginal ultrasound
ct to assess peritoneal, omental and retroperitoneal disease
cytology of ascitic tap
surgical exploration
histopathology
cxr
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178
Q

what is the treatment for ovarian epithelial ca

A

surgery + chemo (cisplatin and paclitaxel)

staging lap/TAH/BSO, debulking

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179
Q

what is the treatment for non-epithelial ovarian ca

A

chemo +/- conservative surgery

palliative

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180
Q

what are the peak ages of incidence of cervical carcinoma

A

30’s and 80’s

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181
Q

what are the histological types of cervical carcinoma

A

2/3 ssc

15% adenocarcinoma

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182
Q

what are the risk factors for cervical ca

A
  • hpv 16/18
  • sti’s
  • young age at first intercourse
  • multiple sexual partners
  • smoking
  • long term use of cocp
  • immunosuppression/hiv
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183
Q

what is CIN

A

premalignant condition to cervical cancer, occuring at the transformation zone
it is asymptomatic

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184
Q

what is the current UK cervical screening programme

A

first invitation at 25
then 3-yearly until 50
50-65 : 5-yearly
after 65 : selected patients only

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185
Q

what is the process for analysing a cervical smear

A

liquid-based cytology - looking at morphology under microscope
dyskaryosis detected, if borderline/mild: further tests for HPV. If +ve - colposcopy in 8/52
if mod/severe - straight to colptoscopy in 4/52
if suspected invasive ca: colposcopy in 2/52
can perform direct biopsy from here which will give a histological diagnoses of CIN invasion

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186
Q

list some of the ways in which cervical ca can present

A
  • IMB
  • PMB
  • PCB
  • blood-stained vaginal dc
    if very advanced: fistulae, renal failure, nerve root pain, lymphoedema
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187
Q

what are the clinical stages for cervical ca

A

1) confined to cervix
2) cervix + upper 1/3 of vagina/parametrium
3) pelvic spread, side wall, lower 1/3 vagina
4) distant spread - invade adjacent organs, distant sites

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188
Q

what are the treatments for cervical ca according to stage

A 
1a) tissue-cone biopsy
1b-2a)radical hysterectomy, chemo/radio
beyond 2a) chemoradiotherapy
post op radiotherapy
lymph node disection
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189
Q

list some of the side effects of radiotherapy for patients with cervical cancer

A

vaginal dryness, stenosis
radiation cystitis, proctitis
loss of ovarian function

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190
Q

which HPV strains are important in cervical cancer

A

16, 18, 31, 33, 45

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191
Q

what levels do the sympathetic and parasymapthetic nerves that supply the bladder come from

A

sympathetic: t12-l2
parasymp: s2-s4
( somatic: s2-s4)

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192
Q

what is classed as nocturia

A

voiding >2 times/night

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193
Q

what gynae history shouldl be taken in a patient presenting with incontinence

A
  • previous births
  • birthweight
  • forceps delivery?
  • episiotomy
  • perineal trauma - grade
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194
Q

what should be examined in a patient presenting with incontinence

A
  • obesity
  • scars
  • abdo/pelvic mass
  • visible incontinence
  • prolapse
  • pelvic floor tone
  • cns
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195
Q

what are some of the quantitative tools that can be done in a patient with incontinence

A
  • urinalysis
  • diaries
  • pad tests
  • uss/iv pyelogram (for renal tract abnormalities)
  • postmicturition uss or catheterisation for residual volume measurement
  • cystoscopy, urodynamics/cystometry
  • axr for calculi
  • methylene dye test for fistulas
  • CT + contrast in some cases to look at integrity of ureter
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196
Q

what parameters can you assess from cystometry

A

bladder capacity, flow rate, voiding function

inserting bladder and PR catheters can measure the difference between abdominal and bladder pressure

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197
Q

list some general advice you can give to someone with incontinence

A

moderate fluid intake, 1,500-2,500ml/day
tea/coffee/alcohol should be reduced/stopped
pelvic floor exercises
commodes/downstairs toilets/bedpans/pads in some

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198
Q

list the treatment options for someone with urodynamic stress incontinence

A
  • pelvic floor exercises with physiotherapy
  • meds e.g. duloxetine
  • urethral injections e.g. collagen, silicone
  • surgery; Burch colposspension; tension free vaginal tape
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199
Q

list the treatment options for someone with detrusor overactivity incontinence

A
  • drugs: anticholinergics, antidepressants e.g. imipramine, oxybutinin, tolterodine (specific for detrusor muscle muscarinic receptors), solifenacin, trospium
  • botulinum toxin injection
  • surgery as last resort e.g. urinary diversion
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200
Q

list the predisposing factors for prolapse

A
  • age
  • menopause
  • parity
  • obesity
  • connective tissue disease
  • smoking
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201
Q

give the symptoms that someone with prolapse can get

A

feeling of “something coming down”, backache or lower abdo pain,
urinary/faecal incontinence, difficulty with micturition
bleeding/discharge
apareunia

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202
Q

what are the treatment options for prolapse

A

if asymptomatic, may choose to do nothing “watchful waiting”
lifestyle: cough management, stop smoking, constipation, weight loss, avoiding heavy lifting
pelvic floor exercises with physio
pessaries to reduce prolapse
surgery (anterior/posterior/anterior and posterior repair depending on type of prolapse)

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203
Q

list some of the complications of surgery for prolapse

A 
recurrence
haemorrhage, vault haematoma
vault infection
dvt
new incontinence
uterine and bladder injury
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204
Q

which structures usually support the pelvic organs

A

levator eni muscles and endopelvic fascia

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205
Q

describe the different types of prolapse

A
  • anterior compartment: urethrocoele, cystocoele, cystourethrocoele
  • middle compartment: uterine prolapse, vaginal vault prolapse, enterocoele (herniation of pouch of douglas)
  • posterior compartment: rectum prolapses into vagina
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206
Q

how would you examine someone with prolapse

A

speculum + pv when lying down; ask them to cough/strain while slowly removing the speculum
both standing and in left lateral position
determine degree of prolapse
pr may be required to check for rectal prolapse

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207
Q

what other problems may prolapse be associated with

A

bowel: constipation, straining, urgency, incontinence, incomplete evacuation
bladder: incontinence, frequency, urgency, incomplete bladder emptying

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208
Q

which procedure is done in bladder/urethral prolapse

A

colposuspension

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209
Q

which procedure is done in uterine prolapse

A

hysterectomy, sacrohysteroplexy, sacrospinous fixation

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210
Q

which procedure is done in recto/enterocoele

A

colporrhaphy

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211
Q

what are some of the complications of a prolapse

A

recurrence despite treatment
ulceration
uti
retention, incontinence (overflow)

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212
Q

define overactive bladder incontinence

A

involuntary urine leakage due to uncontroleed increases in detrusor pressure, increasinf pressure beyond that of the normal urethra

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213
Q

define stress incontinence

A

involuntary leakage of urine due to intraabdominal pressure beyond that of urethre

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214
Q

what does a urinary diary involve

A

patient keeps record of the time and volume of fluid intake and micturition over a week. gives info on drinking habits, frequency and bladder capacity

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215
Q

what do urodynamic tests show in overactive bladder and stress incontinence

A
  • overactive bladder: involuntary detrusor contractions detected on cystometry, causing urine flow
  • stress: increased abdo pressure causes increased bladder pressure and causes urine flow
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216
Q

what is the management for overactive bladder

A
  • lifestyle modifications
  • review drugs affecting bladder
  • bladder training - regularity
  • drugs: anticholinergics/antimuscarinics
  • if postmenopausal, can give oestrogens to reduce effects of atrophy
  • botulinum toxin (blocks neuromuscular transmission)
  • surgery rarely
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217
Q

what is the management of mixed incontinence

A

management according to whether stress inconctinence or overactive bladder symptoms are most bothersome

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218
Q

how can bladder retention cause incontinence

A

chronic retention of urine in the bladder can increase pressures to the level that it eventually cannot be held any longer and causes overflow
(intermittent self catheterisation often required)

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219
Q

what receptors are found in the bladder that are associated with voiding and filling

A

M3 - parasymp - contraction of detrusor muscle: holding
B3 - symp - relaxation of detrusor muscle: filling
a1 : contraction, filling phase; voluntary skeletal muscle

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220
Q

what are the risk factors for candidiasis

A

pregnancy, diabetes, abx, recently, immunocompromise

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221
Q

what are the symptoms of candidiasis

A

“cottage cheese” dc with vulval irritation and itching. superficial dyspareunia and dysuria may occur
vagina/vulva inflamed and red

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222
Q

how is candidiasis diagnosed

A

culture

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223
Q

what is the treatment of candidiasis

A

clotrimazole (canesten) or floconazole

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224
Q

what is the pathophys for bacterial vaginosis (i.e. gardnerella)

A

when normal lactobacilli are overgrown by a mixed flora including anaerobes, gardnerella and mycoplasma hominis

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225
Q

what are the symptoms of bacterial vaginosis

A

grey-white dc but vagina not red or itchy

characteristic “fishy odour”

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226
Q

how is bacterial vaginosis diagnosed

A

increased vaginal pH, typical dc, positive Whiff test (KOH), “clue cells” on microscopy

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227
Q

what are the complications of chlamydia

A

as it is often asymptomatic - can cause chronic pelvic infection with tubal dmaage, subfertility and chronic pelvic pain

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228
Q

what is reiter’s syndrome

A

chalmydia-associated: urethritis, uveitis and arthralgia

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229
Q

what is the diagnostic test for chlamydia

A

NAAT (nucelic acid amplification test - PCR)

urine sample for screening

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230
Q

which antibiotics are used to treat chalmydia

A

7/10 Doxycyline +

1g stat Azithromycin

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231
Q

if there are any symptoms, which symptoms may occur with chalmydia

A

urethritis, vaginal dc

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232
Q

is n. gonorrhoea gram +ve or -ve

A

-ve

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233
Q

what symptoms may occur with gonorrhoea in women

A

commonly asymptomatic, but may have vaginal dc, bartholinitis, urethritis, cervicitis,

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234
Q

what symptoms do men with gonorrhoea develop

A

urethritis, and can cause bacteraemia, monoaticular septic arthritis too systemically

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235
Q

what is the treatment of vaginal warts

A

podylophillin topically or imiquimod cream
alternatively, cryotherapy or electrocautery if resistent
(HPV vaccine may prevent)

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236
Q

which hsv type is most common cause of genital herpes

A

hsv2

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237
Q

what is the presentation of genital herpes

A

multiple small painful vesicles and ulcers around the introitus
local lymphadenopathy, dysuria, systemic symptoms

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238
Q

what type of organism is trichomonas

A

flagellate protozoan

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239
Q

what are the symptoms of trichomoniasis

A

offensive grey-green dc
vulval irritation
superficial dyspareunia

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240
Q

what may the cervix look like on examination of someone with trichomoniasis

A

punctuate, erythematous - “strawberry”

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241
Q

what is the diagnosis of gonorrhoea

A

culture of endocervical swabs ( + sensitivities), NAAT

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242
Q

what is the diagnosis of trichomoniasis

A

wet film, staining, culture of vaginal swabs

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243
Q

what is the treatment for trichomoniasis

A

metronidazole

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244
Q

how does endometritis present

A

can be post pregnancy, sti, TOP, miscarriage, vaginal instrumentation etc
and symptoms include persistent and often heavy vaginal bleeding, pain, tender uterus, os commonly open, may be offensive smelling dc
+/- septicaemia, fever, dc

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245
Q

what is the diagnosis of endomteritis

A

vaginal/cervical swabs
fbc
uss

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246
Q

what is the management of endometritis

A

broad spec abx

erpc

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247
Q

what is the causative organism for syphillis

A

treponema pallidum spirochete

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248
Q

what are the typical symptoms of primary syphillis

A

solitary painless ulcer

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249
Q

what are the typical symptoms of secondary syphillis (untreated)

A

weeks later, often with rash, influenza-like symptoms, condylomata (warty growths), variety of systemic symptoms

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250
Q

what are the typical symptoms of latent syphillis

A

many years later - aortic regurg, dementia, tabes dorsalisskin gummata

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251
Q

what is the diagnosis of syphillis

A

enzyme immunoassay (syphilis EIA)
VDRL test
syphillis serology
test from active lesion

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252
Q

what is the treatment for any stage of syphillis infection

A

penicillin

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253
Q

what are the risk factors for hiv

A

multiple partners, unprotected sex
migration from high-prevalence countries (esp subsaharan africa)
ivdu
msm contact

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254
Q

what are the symptoms of hiv seroconversion if any

A

influenza-like illness, with rash

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255
Q

what is the definition of AIDS

A

development of opportunistic infections or malignancy due to much-reduced CD4+ count (<200 cells/mm^3)

256
Q

what is the aetiology of PID

A

ascending infection of bacteria in the vagina and cervix
can be provoked by instrumentation, TOP, ERPC, , miscarriage. mostly chlamydia/gonorrhoea
(can also occur from descending infections e.g. appendix)

257
Q

what surrounding structures can be affected by PID

A

endometrium (endometritis), salpingitis, parametritis, fitx hugh curtis

258
Q

what are some of the symptoms of PID, if symptomatic

A

subfertility, menstrual problems, chronic pelvic pain, deep dyspareunia is a hallmark, abnromal vaginal bleeding/dc

259
Q

what are some of the signs on examination of PID

A

lower abdo peritonitic signs
adnexal tenderness
“cervical excitation”/”cervical motion tenderness”: painful
abscess may even be palpated pv

260
Q

what is the treatment for PID

A

analgesia: parenteral cephalosporin e.g. IM ceftriaxone, followed by doxycycline or metronidazole

261
Q

what is the treatment for bacterial vaginosis

A

metronidazole and clindamycin cream

262
Q

what is the treatment for gonorrhoea

A

IM Ceftriaxone + 1g stat Azithromycin if suspected

7-day follow-up

263
Q

list some of the complications of PID

A
  • abscess
  • pyosalpinx
  • tubal onbstruction
  • infertility
  • ectopic pregnancy risk increased
264
Q

what happens in chronic PID

A

perisisting untreated infection causing dense pelvic adhesions, obstruction to fallopian tubes, dilation with fluid (hydrosalpinx), pyosalpinx

265
Q

what are the symptoms of chronic PID

A

chronic pelvic pain, dysmenorrhoea, deep dyspareunia, heavy irregular mesntruation, chronic vaginal dc, subfertility

266
Q

how is chronic PID diagnosed

A

TVUS reveals fluid collections in fallopian tubes or surrounding adhesions
laparoscopy is best tool
swabs taken

267
Q

what is the treatment for chronic PID

A

analgesics and abx if active infection (IM ceftriaxone + PO metronidazole)
adhesiolysis and salpingectomy may be required

268
Q

which drug is given as candidiasis prophylaxis

A

fluconazole

269
Q

what are some of the precipitants of bacterial vaginosis

A
  • unprotected sexual intercourse
  • receptive OI
  • perfumed bath products, douching
  • menstruation
    NOT an STI
270
Q

list the examinations for vaginal dc

A
  • examination
  • vaginal ph
  • high vaginal swab (culture, wet mount, gram stain)
  • endocervical swab (NAAT, culture)
  • HSV PCR
271
Q

how can you try and reduce transmission of herpes

A

condoms, avoid sex when lesions present/prodrome, infrom partners if risk, suprressive aciclover, advise to inform partners, avoid oral sex if oral herpes

272
Q

list the treponemal blood tests for syphillis

A
  • EIA - IgG (screening test)
  • TPPA/TPHA (stay positive once exposed)
  • IgM - marker of acute infection
273
Q

what is the follow test for syphillis

A

VDRL

274
Q

list some non-infective causes of ulceration

A

crohn’s
behcet’s
apthous ulcers

275
Q

list the steps in which the HIV DNA replicates

A 
1- HIV attaches to CD4
2- fusion
3- genomic RNA (reverse transcriptase)
4- replication and budding of mature HIV virion
5- nucleic acid detection : RNA/NA
6- EIA
7- HIV genotype
276
Q

discuss some of th einfections more common in patients with AIDS

A
  • bacterial e.g. TB
  • fungal e.g. candidia, pneumocystis
  • viral: HSV, CMV
  • protozoa: toxoplasmossi
  • CNS: encephalopathy
  • malignancy: kaposi sarcoma, cervical
277
Q

list the different virology tests for HIV

A

1) antigen detection (Ag)
2) IgM - first response, transient
3) IgG - subsequent response, may persist

278
Q

how may someone with HIV present

A
  • concerned patient after risky event
  • acute seroconversion illness
  • routine testing - antenatal, AMU, GUM, occy health
  • opportunistic infections/AIDS
279
Q

list some of the features of acute seroconversion illness in HIV infection

A
  • fever
  • malaise
  • arthralgia
  • headache
  • sore throat
  • lymphadenopathy
  • rash
280
Q

how is HIV managed

A

1) HAART
2) HIV monitoring : viral load, CD4 count, genotyping
3) testing for other conditions e.g. Hep B/C
4) treat/prevent opportunistic infections
5) PEP - try to prevent integration of HIV DNA into host DNA

281
Q

what are the different classes of mechanism of action of HAART

A
  • fusion/entry inhibitors
  • protease inhibitors
  • integrase inhibitoes
  • reverse transcriptase inhibitors
    (each affect different parts of HIV replication cycle)
    triple therapy - combines 3 drugs from two different classes to prevent resistance
282
Q

list the symptoms of acute hepatitis B

A

fever, RUQ pain, jaundice
malaise, anorexia/nausea,
dark urine/pale stools
fulminant (transplant)

283
Q

what are the features of the hepatitis virus

A

enveloped, partially dsDNA

284
Q

what does chronic hepatitis B cause

A

cirrhosis of the liver, HCC

285
Q

describe how the hep B antigens/antibody levels vary according to time

A

HBsAg - increases over 4-24 weeks (acute)
total anti-HBc if ever been infected
IgM anti-HBc increases from 4-32 weeks
anti-HBs increases after 32 weeks (immunity)
HBe Ag (marker of infectivity)

286
Q

what is the prevention for Hep B

A

risk factor modification
vaccine 0,1,6 months
neonates: 0/1/2/12 months
post exposure: needlestick, neonates to infected mothers

287
Q

what is the management of Hep B

A

admit if unwell, refer to infectious diseases/hepatology/GUM
notify prevention of infectious disease
full serology testing
baseline liver tests

288
Q

what advice would you give to someone diagnosed with hep B

A

risk of transmission
avoid alcohol
breastfeeding okay if baby immunised
antivirals and referral

289
Q

what is the structure of Hep C

A

enveloped ssRNA

290
Q

what are the clinical features of Hep C

A

usually asymptomatic
20% clear infection
80% have chronic infection - cirrhosis, hcc

291
Q

what are the serology tests for Hep C

A

1- anti-HCV (total) for initial screening
2- Ag
3- Ab
4- HCV RNA (if present: infectious, infected)

292
Q

what is the management of Hep C

A

advice: lose wieght, avoid alcohol, stop smoking
vaccines: hep a/b
if acute: monitor for 3 months to see if it clears itself
drug therapy depends on genotype e.g. interferon and ribavirin is old regime. now, there are many new targeted drugs e.g. sofobuvir, daclatasvir

293
Q

list some of the risk factors for hep a and e

A

travel - africa, asia, south america
msm
ivdu

294
Q

explain the importance of contact tracing in GUM

A

course of infection should be traced in order to treat past contacts and break chain of disease. used for most GU diseases except HIV, providing an anonymous and confidential method of contacting sexual contacts of affected patient.

295
Q

how would you investigate a patient with suspected PID

A 
urine dipstick, msu
pregnancy test
swab
sti screen: NAAT, ELISA
bloods: FBC/U+E/ESR
uss
laparoscopy
mri/endometrial biopsy/doppler flow studies
296
Q

what is the normal frequency of antenatal visits

A
  • for uncomplicated nulliparous: 10
  • for uncomplicated parous: 7
    incorporate routine tests into visits
297
Q

what tests/investigations are done at each antenatal visit

A
  • bp and urine dip
  • from 24 weeks: fundal-symphysis height
  • from 36 weeks: check foetal presentation
  • ## routine ctg
298
Q

describe the foetal anomaly screening in antenatal care

A

normally between 18+0 - 20+6

which allows option to terminate pregnancy, parents to prepare for treatment, specialist care, intrauterine therapy

299
Q

describe screening for down’s syndrome

A

done by end of first trimester (13+6) - combined test of bHCG, PAPPA, nuchal translucency
quadruple test from 14+2 - 20+0: hCG, afp, inhibin A, UE3
cut off of 1/150 for further testing

300
Q

what symptoms would you advise a woman to look out for for preeclampsia

A
  • severe headache
  • visual disturbance
  • severe pain just below ribs
  • vomiting
  • sudden swelling of hands
301
Q

around which week are US anomaly scans done in antenatal care

A

20 weeks

302
Q

what antenatal information is given at the first antenatal visit - booking visit (10 weeks)

A
  • folic acid supplements (400 mcg)
  • nutrition, diet, vit d, food hygiène
  • pelvic floor exercises
  • pregnancy care pathway and place of birth
  • breastfeeding workshops
  • antenatal classes
  • discussion of mental health issues
303
Q

what is examined for at the booking visit of anc

A

height, weight,
bloods taken
rule out hx of fgm
signs of domestic violence

304
Q

which bloods are taken at booking visit of anc

A

hb, rhesus status
ab’s, syphillis, hep b, hiv, rubella
sickle cell/thalassaemias Ihigh risk ethnicities)
gtt if at high risk of diabetes

305
Q

when is a dating scan done

A

between 8 and 14 weeks

306
Q

list the risk factors for gestational diabetes

A
  • bmi>30
  • prev macrosomic baby >4.5kg
  • fhx of diabetes 1st deg relative
  • high risk ethnicity groups
  • htn, preeclapmsia hx
307
Q

what is offered for hep B positive pregnant women

A

post natal intervention for baby

308
Q

at which week/s is anti-D given

A

28 and 34(?)

309
Q

what information is given to woman at 36week anc visit

A 
breastfeeding information
birth plan review
recognition of active labour
care of new baby
newborn screening tests
vit K prophylaxis
post natal self care
awareness of PND
310
Q

list some of the common symptoms of pregnancy

A
  • nausea and vomiting
  • heartburn
  • constipation
  • haemorrhoids
  • vaginal discharge
  • varicose veins
  • backache
  • tiredness
311
Q

how is pregnancy after 41 weeks managed

A

membrane sweep
induction of labour
ctg monitoring

312
Q

what advice is given to women postnatally

A

advice about physical and emotional wellbeing
coping strategies and support
experiencing common health problems
encourage to report concerns

313
Q

what steps can be taken to look after women preconceptually

A 
rubella check +/- vaccine
manage chronic disease
meds review
routine preconceptual daily folic acid
advice on smoking/drinking/drugs
314
Q

what happens at the booking visit (10 weeks) in anc

A

history and examination, risk assessed
LMP
past obstetric - stillbirth, preeclampsia, gestational diabetes
past gynae - smear, subfertility, prev surgery
examination: bmi, bp, abdo exmination, heart auscultation
decisions made about type and frequency of care

315
Q

at how many week’s gestation is the uterus usually palpable

A

12 weeks

316
Q

what is assessed for women 11+0 - 13+6 weeks antenatally

A

crown rump length
uss - detect multiple pregnancy, chromosomal abnormalities, nuchal translucency scan in conjunction with combined test: Bhcg, PAPPA

317
Q

list the medical conditions it is important to ask about in anc

A 
htn, diabetes, cvs disease
vte, autoimmune disease, haemoglobinopathy
renal disease
depression/mental health
(+ any medications they are on)
318
Q

who is advised for vit D administration in anc

A

bmi > 30
certain ethnicities: south asian, afrocaribbean descent
those found to be vit d deficient

319
Q

what lifestyle advice would you give to a pregnancy woman

A
  • stop smoking/alcohol/elicit drug use
  • well balanced diet (around 2500 kcal)
  • coitus not CI unless rupture of membranes or placenta preavia
  • only use pasteurised milk, avoid soft and blue cheeses, well cooked food
  • avoid contact sports
  • seat belt worn above the bump
320
Q

what is the preparation for the run up to birth in antenatal care

A
  • antenatal classes
  • informed choice about intrapartum and postpartum care
  • intrapartum techniques for posture, breathing, and pushing
321
Q

what week is gtt done in patients with increased risk of gestational diabetes in anc

A

28

322
Q

how is VTE prophylaxis managed in pregnant women

A

weight and risk factors taken into account - if 3 or more (?) present, put on prophylactic sc lmwh injections
prophylactic dose calculated acocrding to booking weight

323
Q

when do pregnant women on vte prophylaxis stop taking it

A

24 hours prior to c-section

onset of labour

324
Q

how long is vte prophylaxis continued post partum

A

up to 6 weeks

325
Q

at how many weeks are results of antenatal screening tests reviewed

A

16

326
Q

if the antenatal downs screening test is missed, what are the women offered

A

triple/quadruple test

327
Q

what happens at the 28 weeks antenatal visit

A

fundal height is measured, fbc and antibodies checked
gtt if indicated
anti-D given in Rh-ve women

328
Q

what is checked at 31 week anc

A

blood results from 28 week appointment

329
Q

what is done in 36, 38 and 40 week anc

A

fundal height measured, lie of foetus, presentation checked, (referred for ecv if breech)

330
Q

what is done at 41 week anc

A

fundal height measured, foetal lie and presentation checked,
membrane sweep offered, and induction of labour offered at 42 weeks

331
Q

what vaccines may be offered to women during pregnancy

A
  • flu vaccine

- whooping cough (pertussis) during weeks 28 and 38 of pregnancy

332
Q

outline the antenatal care management of women with diabetes in pregnancy

A

(+ve urine dip for glucose or gtt may alert you)
- refer to diabetes and antenatal clinic
- assessment of blood glucose control every 1-2 weeks
- offer retinal assessment at 16 weeks
- 20 week anomaly scan
- 36 week advice about birth
(advise that they may be at higher risk of developing diabetes later in life)

333
Q

what advice can be given to a woman preconceptually

A

explain importance of establishing good glycaemic control
offer self-monitoring of glucose levels
dietary advice, weight loss,
folic acid to prevent ntd’s

334
Q

list some of the ways in which gestational diabetes is managed

A 
regular monitoring
dietary changes
metformin
(isophane) insulin 
discontinue any other glucose lowering drugs
335
Q

what parameters are used to diagnose gestational diabetes

A
  • fasting plasma glucose 7mmol/l or more

- 2-hr plasma glucose 7.8mmol/l or more

336
Q

what is the risk associated with gestational diabetes during labour

A

shoulder dystocia

337
Q

what can congential abnromalities be due to

A

inherited defects
chromosomal abnormalities
intrauterine infection
drug exposure, teratogens

338
Q

what marker is raised in ntd’s

A

afp

339
Q

which trisomies are screened for antenatally

A

21, 13, 18

340
Q

describe amniocentesis

A

a diagnostic test, where there is removal of amniotic fluid with the use of a fine guage needle under us-guideance.
it enables prenatal diagnosis of congenital abnormalities

341
Q

what is the miscarriage risk in women undergoing amniocentesis

A

1%

342
Q

describe chorionic villous sampling

A

biopsy of trophoblast by passign a fine-guage needle through abdo all or cervix into the placenta after 11 weeks
used to diagnose chromosomal problems,

343
Q

list the risk factors for down’s syndrome

A
  • high maternal age
  • prev affected baby
  • thickened nuchal tranparency. structural abnormalities, shortened nasal bone, tricuspid regurg on uss
344
Q

what is the pathophysiology of ntd’s

A

failure of closure of neural tube - causes neural tube tissue to often be exposed, causing degeneration
spina bifida and anencepahly are most well known forms

345
Q

what is the normal dose of folic acid given to pregnant women in first trimester/preconceptually in order to prevent ntd’s

A

0.4mg/daily

346
Q

what is the in utero treatment for babies with arrhythmias

A

flecainide, digoxin

347
Q

what can diaphragmatic hernias in babies cause as a consequence

A

pulomnary hypoplasia

348
Q

list some gi defects that can occur in foetuses

A
  • gastroschisis, exomphalmos
  • oesophageal atresia and tracheooesophageal fistula
  • duodenal atresia (double bubble sign)
  • lower gut atresia (dilated bowel)
349
Q

list the causes for foetal hydrops

A

1) immune - anaemia, haemolysis (rh disease)
2) chromosomal abnormalities e.g. trisomy
3) pleural effusions/other structural abnormlaities
4) cardiac - abnormlaities, cardiac failure
5) twin-twin transfusion syndrome

350
Q

how is foetal hydrops investigated

A 
uss, echo
mca assessment
maternal blood for kleihauer test
foetal blood sampling
amniocentesis for karyotyping
351
Q

when is a baby considered small for date/small for gestational age

A

<10th centile

352
Q

what is foetal distress

A

acute situation such as hypoxia, in which normal growth and development are not optimal

353
Q

what is foetal compromise

A

chronic situation when conditions of normal growth and development are not normal

354
Q

what is placental dysfunction

A

poor nutrient transfer across placenta - commonly there is iugr

355
Q

list some of the methods of foetal surveillance

A

1) symphysis-fundal height
2) uss
3) doppler umbilical waveform
4) doppler waveform of foetal circulation looking at major foetal vessels e.g. mca
5) hfr, ctg
6) ask if kicking/movements are normal

356
Q

list some of the causes of sga/iugr

A 
consitiutional
preexisting maternal disease, maternal pregnancy complication e.g. preeclampsia, multiple pregnancy
smoking, durgs, alcohol
infections e.g. cmv
malnutrition
357
Q

how is sga investigated

A 
uss 
doppler umbilical artery
mca blood flow
ctg
oligohydraminos?
358
Q

how is sga managed

A
  • if small but consistently-gorwing with normal investigations, leave alone
  • if abnormal investigations at term - c section or induction
  • if preterm and abnormalities - admit and monitor, give steroids, deliver beyond 34 weeks
359
Q

when is a pregnancy classed as “prolonged”

A

42 weeks or more

360
Q

what is the risk of prolonged gestation

A

increased risk of stillbirth, foetal distress

361
Q

list some of the risk factors that may prompt you to give vte prophylaxis antenatally and for 7 days after delivery
(3 or more risk factors)

A 
age > 35
mbi >30
parity >4
varicose veins
immobility
certain medical disorders
dehydration/excessive blood loss
surgery in pregnancy
long haul travel
preeclampsia
midcavity instrumental delivery
prolonged labour
362
Q

list the risk factors that would prompt you to give vte prophylaxis antenatally and for 6 weeks after delivery

A
  • prev vte
  • lupus
  • protein c/s deficiency
  • factor v leiden, or prothrombin gene
  • antithrombin deficiency
363
Q

list some of the symptoms that may be found in the history of someone with ectopic pregnancy

A
  • rif/lif pain
  • irregular pv spotting/bleeding
  • fainting, dizziness
  • shoulder tip pain
364
Q

list the risk factors for ectopic pregnancy

A
  • previous ectopic pregnancy
  • tubal surgery
  • tubal pathology
  • prev pid/endometriosis
  • iucd, pop if fails
365
Q

list some of the site, apart from tubal ,where an ectopic pregnancy can implant

A

ovarian, abdominal, uterine scar

366
Q

what is the management of ectopic pregnancy

A
  • methotrexate if criteria met

- surgery if medical criteria not met/ clinically unwell: laparoscopy/laparotomy -> salpingectomy/otomy

367
Q

what is the definition of recurrent miscarriage?

A

loss of 3 or more consecutive pregnancies

368
Q

list some of the causes for recurrent miscarriage

A
  • chromosomal abnormalities
  • genetic defects
  • antiphospholipid syndrome, other rheum conditions
369
Q

what is the management of miscarriage

A

conservative, medical or surgical

conservative: waiting for products of conception to pass naturally, with 24 hr access to gynae service
medical: day 1 mifepristone and day 3 misoprostol
surgical: evacuation of retained products of conception (erpc) - use of suction curette to empty uterus; alternatively dilation and curettage

370
Q

what are the adv and disadv of conservative management of miscarriage

A

adv: avoids risk of surgery/medication
disadv: pain and bleeding can be unpredictable, takes longer, may be unsuccessful

371
Q

what are the adv and disadv of medical management fo ectopic pregnancy

A

adv: avoids surgical complications and high patient satisfaction if successful. can be done as outpatient
disadv; pain and bleeding may be unpleasant

372
Q

what are the adv and disadv of surgical managment of ectopic pregnancy

A

adv: provides closure, planned procedure

disadv; surgical/anaesthetic, perforation, bowel/bladder/cervix damage, asherman’s, cervical weakness

373
Q

what is a threatened miscarriage

A

bleeding and pain up to 24 weeks with a viable ongoing pregnancy. cervical os closed

374
Q

what is an inevitable miscarriage

A

cervical os open

poc have not yet been passed, but they inevitably will

375
Q

what is an incomplete miscarriage

A

com poc have been passed, but some clots and tissues remain within the uterus
cervical os open
(if infected -> septic)

376
Q

what is a complete miscarriage

A

all products of conception have been passed, and bleeding and pain start reducing. cervix is now closed (uss shows empty cavity)

377
Q

what is the aetiology for miscarriage

A

most cases cause is not established
chromosomal abnormalities, congenital abnormalities
maternal disease, uterine abnormalities, acute illness/infection, poorly controlled diabetes, thrombophilia/antiphospholipid synd

378
Q

what are the risk factors for miscarriage

A 
advanced maternal age
previous miscarriage
smoking, alcohol, drugs
folate deficiency
consanguinity
379
Q

what is trophoblastic disease

A

spectrum disorders arising from disorders of trophoblastic development arising from abnormal implantation

380
Q

what is the presentation for trophoblastic disease

A
  • bleeding/haemorrhage
  • severe nausea and vomiting
  • uterus large for dates
381
Q

what is the risk associated with trophoblastic disease

A

potentially premalignant - molar pregnancy, hydatidiform mole, complete mole -> can become invasive mole/choriocarcinoma

382
Q

what is the management of trophoblastic disease

A

surgical erpc

register with one of the three national gestational trophoblastic disease centres

383
Q

how can you manage the psychological implications of miscarriage

A

give info/leaflets
encourage discussion
counselling and support

384
Q

what are the features of true hyperemesis gravidarum

A

severe dehydration, deranged bloods, marked ketosis

weight loss and nutritional deficiency may be a feature

385
Q

at which weeks of gestation does hyperemesis gravidarum usually occur

A

6-20

386
Q

what investigations would you order in a patient with hyperemesis gravidarum

A
  • urine: pt/ketones/uti
  • fbc: haematocrit
  • U+E: K+ especially
  • lft/amylase
  • tft
  • uss to exclude trophoblastic disease, multiple pregnancy
387
Q

what is the management for hyperemesis gravidarum

A
  • rehydration - not with glucose
  • thiamine replacement
  • antiemetics parenterally
  • ranitidine
  • thromboprophylaxis
  • rarely: steroids
388
Q

list the different types of miscarriage

A
  • threatened
  • inevitable
  • incomplete
  • complete
  • septic
  • missed
389
Q

what is a missed miscarriage

A

foetus has not developed, or has died in utero. this si not recognised however by the body, and it carries on “thinking it’s pregnant”. os closed

390
Q

how are missed miscarriaged picked up

A

uss, bleeding occuring eventually

391
Q

what investigations are carried out in miscarriage

A
  • uss to show foetus in uterus or not, and if viable
  • hcg blood levels (increases in viable pregnancy, then plateus once very high)
  • fbc and rhesus group
392
Q

what can be given to prevent bleeding in miscarriage

A

ergometrine

393
Q

what is done with a viable foetus with threatened miscarriage

A

no intervention proven to prevent miscarriage

394
Q

what are the complications of miscarriage

A

heavy pv bleeding
shock - causes multisystem failure
ashermans syndrome

395
Q

how should you counsel a patient who has had a miscarriage

A

tell them that the miscarriage is not a result of something they did or didnt do
could not have been pregnant
reassure that there is a high chance of successful further pregnancies
referral to support group e.g. miscarriage association
only further investigations if recurrent

396
Q

list some of the grounds for which a termination of pregnancy is acceptable

A

continuance of pregnancy would be a risk to life of pregnant woman, would cause permanent physical or mental health problems
pregnancy not exceeded 24 weeks and continuance would involve risk
substantial risk that is child were born it would suffer from physical and mental abnormalities

397
Q

what are the methods of TOP

A

bloods: taken for hb, blood group, rhesus status, haemoglobinopathy
medical: mifepristone + misoprostol/gemeprost
surgical: curettage, dilatation and evacuation (with antibiotic cover)

398
Q

what is the mechanism of action of mifepristone

A

antiprogesterone

399
Q

what is the mechanism of action of misoprostol

A

prostaglandin

400
Q

what are the complications of TOP

A

haemorrhage, infection, uterine perforation, cervical trauma, failure, psychological sequelae

401
Q

what may be found on examination of a woman with ectopic pregnancy

A
  • tachy
  • hypotension
  • collapse
  • usually abdo and often rebound tenderness
  • movement of cervix o/e can cause pain
  • adnexa may be tender
402
Q

what investigations would you do in someone with suspected ectopic

A
  • pregnancy test - urine hcg
  • uss (preferably tvus) may or may not be able to visualise the pregancy, can show free fluid in the abdomen
  • quantitative serum hcg: slower-rising or lower levels in ectopic compared to viable
  • laparoscopy
403
Q

how do you monitor if treatment for ectopic pregnancy has worked

A

hcg levels should fall

404
Q

can you treat a ruptured ectopic with medical management

A

no

405
Q

which antiemetics are given in hyperemesis gravidarum

A
  • cyclizine
  • metoclopramide
  • ondansetron
406
Q

how is herpes zoster managed in affected pregnant women

A

immediate po acicolovir

chicken pox can be teratogenic

407
Q

what can parvovirus in utero cause

A

suppressed erythropoeisis: anaemia

408
Q

what are the risks of group B strep in pregnancy

A

neonate can become infected after membrane rupture, especially if preterm

409
Q

what is given to prevent vertical transmission of group B strep in pregnancy

A

iv pencilllin

410
Q

which infections are screened for in TORCH screen

A
  • toxoplasmosis
  • rubella
  • cmv
  • herpes simplex
411
Q

what can result from infection of a pregnant woman with cmv

A

childhood handicap, deafness

412
Q

what is the management for herpes simplex in pregnancy

A

referral to gum clinic
woman needs aciclovir in late pregnancy
neonate may require aciclovir if exposed
c-section recommended if attack delivery within 6 weeks of attack

413
Q

what are the complications of rubella in pregnancy for the baby

A

deafness, cardiac disease, eye problems (cataracts)

414
Q

what is the management of rubella in pregnancy

A

mother offered termination if infected early in pregnancy

screening at booking

415
Q

what is the causative organism for toxoplasmosis

A

protozoa toxoplasma gondii

416
Q

what are the effects of toxoplasmosis in pregnancy for the baby

A

mental retardation, convulsions, spasticities, visual impairment

417
Q

what is the management for toxoplasmosis in pregnancy

A

education to avoid infection

spiramycin

418
Q

what is the definition of gestational hypertension

A

new hypertension, bp > 140/90, after 20 weeks of gestation

419
Q

what is the definition of preeclampsia

A

hypertension and proteinuria appearing in second half od pregnancy, with/without oedema

420
Q

what is the definition of preexisting hypertension in pregnancy

A

high bp either before pregnancy, or before 20 weeks gestation, or woman already on antihypertensive medicine

421
Q

what is the only cure for preeclampsia

A

delivery

422
Q

what is preeclampsia thought to be due to

A

increased vascular resistance causing htn
increased vascular permeability causing proteinuria
reduced cerebral perfusion -> eclampsia

423
Q

what are the principal risk factors for preeclampsia

A

1) nulliparity
2) previous hx
3) fhs
4) older maternal age
5) chronic hypertension
6) diabetes
7) twin pregnancies
8) autoimmune disease
9) renal disease
10) obesity

424
Q

how is preeclampsia investigated, apart from bp

A
  • urine dip
  • protein:creatinine ratio
  • 24 hour collection of urine
  • bloods (hellp): fbc, U+e, lfts, platelet count, clotting
  • ctg, doppler umbilical artery
425
Q

how may preeclampsa present

A

usually asymptomatic - but headaches, drowsiness, visual disturbance, nausea, vomiting, epigastric pain at later stage

426
Q

what may be found on examination of a patient with preeclampsia

A

increased bp
oedema
epigastric tenderness
urine dipstick for positive proteins

427
Q

what are the maternal complications for preeclampsia

A 
grand mal seizures (eclampsia)
cerebrovascular haemorrhage
HELLP syndrome (liver and coagulation problems)
renal failure
pulmonary oedema
428
Q

how are gran mal seizures from eclampsia treated

A

magnesium sulphate, intensive surveillance

429
Q

what are the foetal complications of preeclampsia

A
  • increased morbidity and mortality
  • iugr if 34 weeks
  • placental abruption
  • preterm birth
  • hypoxia/distress
430
Q

what are the components of HELLP syndrome, which can result as a complication of preeclampsia

A
  • haemolysis
  • elevated liver enzymes
  • low platelet count
431
Q

what can occur as a result of HELLP syndrome

A

dic
liver rupture
liver failure

432
Q

what can be given to women at risk of preeclampsia

A

aspirin to help placental function, from 16 weeks gestation

433
Q

what warrants admission in preeclamptic women

A
  • symptomatic
  • 2+ protein on dip
  • bp >160/110 (severe preeclampsia)
  • suspected foetal compromise
434
Q

which antihypertensive drugs can be given to women with preeclampsia

A
  • labetolol
  • methyldopa
  • nifedipine
    (magnesium sulfate for treatment/prevention of eclapmsia)
  • steroids may be given if baby <37 weeks?
435
Q

when is labetolol contraindicated for preeclampsia

A

if woman has asthma

436
Q

what are the rules for monitoring, admitting or delivery for preeclampsia

A
  • if just htn - monitor for foetal compromise and induce by 40 weeks
  • mild preeclampsia - deliver at 37
  • severe preeclampsia - steroids if <37, admission and surveillance, ctg, fluid balance, frequent blood testing
  • if severe preeclampsia + complications/foetal distress - deloivery whatever the gestation
437
Q

describe the postnatal care that should be given to women with preeclampsia

A
  • may worsen during this time
  • monitor liver enzymes, platelets, and renal function closely (low platelets usually return to normal within a few days)
  • fluid balance monitoring essential
  • cvp monitoring may be required
  • bp maintained at around 140/90
  • b blockers, nifedipine, acei postpartum
  • bp monitoring after dc
438
Q

list some of the complications after eclampsia for the foetus

A
  • placental abruption
  • stillbirth
  • iugr
  • miscarriage
439
Q

list some of the foetal complications of gestational diabetes

A
  • increased risk of congenital abnormalities, and cardiac defects
  • preterm labour
  • macrosomia
  • polyhydramnios
  • dystocia and birth trauma
  • foetal compromise, distress, sudden death
440
Q

what are the maternal consequences of gestational diabetes

A
  • increased preeclampsia risk
  • retinopathy often worsens
  • hypos/dka if not well controlled
  • infections more likely after delivery
441
Q

what is the monitoring for gestational diabetes

A

uss to monitor foetal growth and size
umbilical artery doppler if preeclampsia
retina screen, renal function screen
apsirin daily to reduce risk of preeclampsia

442
Q

what is advised in terms of delivery for gestational diabetes

A
  • deliver by 39 weeks

- if > 4kg, c section

443
Q

what may be the complications of a neonate born to a mother who had gestational diabetes

A
  • hypoglycaemia

- respiratory distress

444
Q

how is gestational diabetes detected

A

at 28 weeks with gtt, if risk factors present

445
Q

what are the risk factors for developing gestational diabetes

A
  • high bmi
  • previous large baby
  • first degree relative with diabetes
  • unexplained stillbirth
  • certain ethnicites e.g. afrocaribbean, south asian, middle eastern
446
Q

is warfarin given in pregnancy

A

no -teratogenic

447
Q

how should pregnant women with epilepsy be managed

A

antiepileptic drug review - ideally preconceptually
avoid sodium valproate
lamotrigine and carbamazepine and (keppra?) are safe in pregnancy
folic acid supplements

448
Q

how should a pregnant woman with thyroid problems be managed

A

replacement with thyroxine
ptu for hyperthyroidism kept at lowest possible dose as it crosses the placenta
post partum thyroiditis can increase risk of pnd

449
Q

what are the obstetric complications of antiphospholipid syndrome

A
  • placental thrombosis
  • recurrent miscarriage
  • iugr
  • early preeclampsia
450
Q

how are pregnant women with antiphsopholipid syndrome managed

A

aspirin and lmwh
serial uss
elective induction of labour at term
postnatal anticoag to prevent vte

451
Q

list some prothrombotic diseases that can affect pregnancy

A

protein c/s deficiency
factor v leiden
(both treated like antiphospholipid syndrome, especially inportant to anticoagulate)

452
Q

how is renal disease in pregnancy managed

A

screening for uti’s
uss foetal growth
measure renal function
control htn

453
Q

how soon after delivery can postpartum thromboprophylaxis be started

A

24 hours if not haemorrhaginf

454
Q

which conditions does high bmi predispose to in pregnancy

A

vte
gestational diabetes
preeclampsia
macrosomia, miscarriage, prematurity

455
Q

what is the management of high bmi pregnancies

A
  • high dose preconceptual folic acid
  • vit d recommended
  • thromboprophylaxis considerations
456
Q

what may be considered in pregnant women who are using illegal drugs

A

mdt, social support

care order in some

457
Q

what are the types of anaemia in pregnancy

A
  • physiological/dilutional
  • iron deficiency
  • folic acid and b12 deficiency
  • sickle cell disease
  • thalassaemia
458
Q

how are hiv-infected pregnant women managed

A 
referral to specialist regional centre
haart - especially zidovudine
c section instead of vaginal birth
do not breastfeed
intrauterine events e.g. ecv are avoided
459
Q

what is the definition of preterm delivery

A

if it occur between 24-37 weeks gestation

460
Q

list the complications of preterm delivery

A
  • prematurity and its complications for the baby
  • infection
  • endometriosis
461
Q

list the aetiology behind preterm delivery

A
  • factors within the placenta e.g. multiple pregnancy, preeclampsia, polyhydramnios
  • iugr
  • infection
  • structural problems e.g. uterine abnormalities, fibroids, congenital abnormalities
  • cervical weakness/ “incompetence”
462
Q

what does antenatal infection cause

A
  • offensive liqour, chorioamnionitis
  • neonatal sepsis
  • endometritis
463
Q

what are the risk factors for antenatal infection

A

bacerial vaginosis

group b strep infection

464
Q

how may preterm delivery be prevented

A
  • cervical suture insertion if cervical incompetence
  • progesterone suppositories
  • screening and treatment of stis and infections
  • amnioreduction for polyhydramnios
465
Q

what investigations would you order in a patient with preterm delivery

A
  • ctg
  • tvus of cervical length
  • high vaginal swabs to look for infection with sterile speculum (be careful as passing speculum is not always indicated)
466
Q

what is the management of preterm delivery

A
  • steroids before 34 weeks
  • delivery - vaginal prefered, c section if obstruction
  • forceps rather than ventouse detected
  • abx for delivery
467
Q

what is the definition of preterm rupture of membranes

A

membrane rupture <37 weeks gestation

468
Q

list the complications of PPROM

A
  • preterm delivery
  • infection of foetus or placenta (chorioamnionitis, endometritis, sepsis)
  • prolapse of umbilical cord
469
Q

why should you avoid a pv/speculum examination in a patient with PPROM

A

avoid introducing infection

470
Q

what are the symptoms/signs of chorioamnionitis

A

contractions, abdo pain, fever, tachy, uterine tenderness, coloured or offensive liquor

471
Q

what are the investigations you would do on someown with pprom

A
  • baby monitoring: ctg, fhr, uss doppler
  • high vaginal swab - fbc, crp
  • amniocentesis for chorioamnionitis
  • DO NOT perform pv examination as you could introduce infection
  • sterile speculum examination in some cases
  • look for amniotic fluid draining
472
Q

what is the management for pprom

A

balance of risk of preterm delivery
admission onto ward, close maternal and foetal surveillance
give steroids
prophylactic erythromycin
if chorioamnionitis - give imediate iv abx and deliver

473
Q

list the risk factors for pprom

A 
smoking, ilicit drug use
previous preterm delivery
pv bleeding any time during pregnancy
lower genital tract infection
multiple gestation
cord prolapse, abruption
474
Q

why is group b strep infection important in pregnancy

A

significant cause of severe early onset infection in newborns

475
Q

is there screening for gbs in pregnancy

A

no - not proved effective

however if detected on high vaginal swab/ previous infection in pregnancy, can give abx in later stages of pregnancy

476
Q

what is the treatment of gbs in pregnancy if positive

A

benzylpenicillin

477
Q

what are the complications of pprom

A
  • prematurity
  • sepsis
  • umbilical cord prolpase
  • stillbirth
  • placental abruption
  • pph/haemorrhage
  • infection
478
Q

what are the different types of chrionicity and zygosity

A

dizygotic: different oocytes, different sperm
monozyogtic: mitotic division of zygote into identical twins
dichorionic diamniotic: two separate placentas and amnions
monochorionic diamniotic: shared placenta, separate amniotic sacs
monochorionic monoamniotic: shared placenta and shared amniotic sac

479
Q

what are the antipartum complications associated with multiple pregnancy

A

maternal: gestational diabetes, preeclampsia, anaemia
foetal: mortality, longer term handicap risk, preterm delivery, iugr, miscarriage, co-twin death

480
Q

describe what twin twin transfusion syndrome is

A

only in monochorionic diamniotic twins - results from unequal distribution of blood through anastomoses of shared placenta
the “donor” is volume deplete and develops iugr, whereas “recipient” gets volume overload

481
Q

what are the more common intrapartum risks in twin pregnancies

A

malpresentation
foetal distress
pph

482
Q

what is the antepartum management of twin pregnancy

A

pregnancy considered high risk

  • iron and folic acid
  • screening for chromosomal abnormalities
483
Q

what is the intrapartum management of twin pregnancy

A

c-section offered or induction at 37-38 weeks
foetal monitoring with ctg
ecv can be performed in second twin if not in longitudinal lie
after delivery, propylactic oxytocin due to risk of pph

484
Q

what is propess

A

prostaglandin pessary given to help induce labour

485
Q

what are the complications with twin pregnancy in first trimester

A
  • hyperemesis, increased miscarriage risk, anaemia
486
Q

what are the complications of twin pregnancy in second trimester

A
  • iugr, tts, gestational htn, diabetes, anomalies, preeclampsia, oligo/polyhydramnios, cord entalngement
487
Q

what are the complications of twin pregnancy during / peri-delivery

A

aph/pph
stillbirth
preterm delivery, preterm labour
abruption

488
Q

what is the definition of antepartum haemorrhage

A

bleeding from genital tract after 24 week’s gestation

489
Q

what are the main causes of aph

A
  • unknown
  • placenta preavia
  • placental abruption
490
Q

describe placenta praevia

A

occurs when the placenta is implanted in the lower segment of the uterus
(classified by proximity of placenta to cervical os)

491
Q

what are the complications of placenta praevia

A

aph
pph
obstruction of foetal head engagement therefore needing c section

492
Q

what is associated with placenta praevia

A
  • intermittent painless bleeds
  • breech presentation
  • abnormal lie
  • foetal head not engaged
493
Q

should you attempt a pv in someone with placenta praevia

A

no -can cause bleeding

494
Q

what are the investigations for placenta praevia

A
  • fbc, clotting, x match
  • ctg
  • uss
495
Q

what is the management for placenta praevia causing aph

A
  • admission due to risk of massive haemorrhage
  • anti D if rh-ve
  • have appropriate bloods on the ready for transfusion if needed
  • steroids if < 34 weeks
  • c section delivery if term/emergency
496
Q

describe what placental abruption is

A

part or all of the placenta separates before delivery of the foetus
significant maternal haemorrhage can occur behind the placenta

497
Q

is bleeding always obvious in placental abruption

A

no - because some of it can clot behind where the placenta separates therefore does not always present with pv bleeding

498
Q

what are the presenting features of placental abruption

A

painful bleeding
bear in mind bleeding not always seen
tachy/other signs suggesting shock
uterus tender and often contracting “woody”

499
Q

what are the risk factors for placental abruption

A 
prev hx
iugr
preeclampsia
htn
maternal smoking
500
Q

how is placental abruption usually diagnosed

A

on clinical grounds

uss may not detect the placenta praevia and can blood clot be mistaken for placenta

501
Q

what is the management for placental abruption causing aph

A
  • resuscitation
  • blood transfusion considered
  • anti d if rh-ve
    c-section if foetal distress
    if no foetal distress and over 37 weeks - induction
    steroids if <34 weeks and no foetal distress, with minimal abruption
502
Q

what is the definition of foetal lie

A

relationship of ofetal long axis to the long axis of the uterus

503
Q

what are the different presentations of a foetus

A

cephalic, breech, other body part

504
Q

list some causes of frequently-changing foetal lie

A

polyhydramnios
multiparity - lax uterus
associated with placenta praevia

505
Q

what are the complications of abnormal lie

A

if head or breech cannot enter the pelvis, labour cannot deliver the foetus.
an arm or umbilical cord may prolapse when the membranes rupture - and can cause uterine rupture eventually

506
Q

what is the management of abnormal lie

A

if <37 weeks, no management unless woman is in labour
if in labour, admit
if >37 weeks, usually admitted to hospital in case membranes rupture - will need to be monitored and need medical input to deliver
the abnormal lie may stabilise itself, and ecv usually doesnt work

507
Q

how is abnormal lie and breech investigated

A

head usually palpated at fundus, or elsewhere not in lower uterus
uss confirms position of baby
uss to look for placenta praevia

508
Q

what are the complications of breech presentation

A 
will often require c-section
head entrapment can cause foetal death
fetal abnormalities more common
cord prolapse
intracranial haemorrhage, internal injuries
509
Q

describe external cephalic version

A

attempt made to turn baby to cephalic presentation, with about 50% success rate
performed in hospital under uss guidance, with a ctg straight after
cannot be done if memrbanes have already ruptured

510
Q

what is given when ecv is performed

A

anti d if rh-ve

511
Q

is ecv usually safe

A

yes - very few will require emergency c section

those who are rh-ve will reuiqre anti-d as a precaution

512
Q

when is ecv contraindicated

A

compromised foetus, membranes ruptured, aph, where vaginal delivery is contraindicated

513
Q

how is breech managed

A

ecv may be tried, but if this fails/is ci’d then you can deliver by c-section
very few delivered vaginally

514
Q

why is it important to catheterise a woman whom you are going to perform a c-section on

A

must empty the bladder first - ensure that it is small and less likely to be damaged during a csection
also if they are under spinal/epidural they are less likely to feel the sensation of needing to void

515
Q

what is the definition of labour

A

progressive effacement and dilatation of the cervix

516
Q

what is “show” in labour

A

cervical mucus plug - white or pinkish in colour

517
Q

what is the 1st 2nd and 3rd stage of labour

A

1st: onset of labour to full dilatation
2nd: full dilatation to delivery of foetus
3rd: delivery of foetus to explusion of placenta

518
Q

how long should the 3rd stage of labour be

A

up to 30 mins

519
Q

which factors affect labour in women

A
  • passage: bony and soft tissues
  • powers: contraction rhythm and strength
  • passenger: size, lie, attitude
520
Q

what is the “attitude” in which a baby presents during labour

A

relation of foetal head to trunk (e.g. flexed, indifferent, deflexed)

521
Q

what is the “position” in which a baby presents during labour

A

relation of foetal “denominator” e.g occiput, mentum, etc, to the maternal pelvis
e.g. - occipito-anterior, occipitoposterior, occipitotransverse position

522
Q

what is the “presentation” of a foetus

A

part of the foetus lowermost in the uterus e.g. cephalic, vertex, brow, face, breech, shoulder etc

523
Q

what are the steps in the mechanism of labour

A
  • engagement
  • flexion
  • descent
  • internal rotation
  • extension
  • external rotation
524
Q

what is the monitoring you would undertake in labour

A

maternal: obs, hydration status, pain, bladder, position
progression: contractions, dilatation, descent of presenting part
3rd stage: bleeding
foetal: heart monitoring, colour of liqour

525
Q

what is the management of 3rd stage of labour

A

oxytocics, ergometrine
controlled cord traction
perineum

526
Q

list the common problems occurring in labour

A
  • failure to progress
  • malpresentation/malposition
  • suspected foetal compromise
  • vbac
  • operate delivery
  • shoulder dystocia
527
Q

what are the “powers”-related causes of failure of progression of labour

A
  • insufficient uterine activity/tone
  • hypotonic ocntraction
  • incoordinate contractions
  • exhaustion, dehydration
528
Q

what are the “passage”-related causes of failure of progression of labour

A
  • abnormal bony pelvis
  • cervical dystocia
  • rigid perineum
529
Q

what are the “passenger”-related causes of failure of progression of labour

A
  • macrosomia
  • abnormal attitude, presentation or position
    (occipitoposterior malpositioning)
530
Q

what is the management for ‘powers’- related failure to progress

A

hydration, analgesia,
amniotomy
oxytocin infusion
delivery by other means if appropriate

531
Q

what is the management of “passage”- related failure to progress

A

c-section

episiotomy if perineum rigid

532
Q

what is the management of ‘passenger’-related failure to progress

A

c-section

instrumental delivery

533
Q

what are the ways in which to induce labour

A

1) membrane sweep
2) prostaglandin e2 (propess) - slow release prostaglandin pessary
3) amniotomy (arom)
4) syntocin (oxytocin)
5) if miscarriage - mifepristone + misoprostol

534
Q

what signs/investigation findings would alert you to foetal compromise

A
  • passage of meconium
  • non-reassuring ctg
  • foetal scalp bloods showing acidosis to confirm
535
Q

what are the features of a non-reassuring ctg

A
  • baseline tachy/brady
  • decreased beat to beat variability
  • absence of acceleration
  • presence of decelerations (below baseline, take a long time to pick up etc)
536
Q

list the causes of foetal compromise in labour

A
  • uterine hyperstimulation e.g. iatrogenic
  • hypotension
  • poor foetal tolerance of labour e.g. iugr
  • cord compression
  • infection
  • maternal disease
537
Q

what is the management for foetal compromise in labour

A

rectify possible causes e.g if maternal hypotension, can put her in left lateral position
stop oxytocics
foetal blood scalp sample
deliver by speediest route if unable to correct acidosis

538
Q

what is the overall success rate of successful vaginal birth after c section

A

70%

539
Q

what are the risks associated with vbac

A
  • need to convert to c section

- uterine scar dehiscence/rupture

540
Q

what are the precaution steps/ investigations done for vbac patients

A
  • iv access, g+s
  • continuous electrical foetal monitoring
  • avoid prolonged labour
  • senior should make decision about whether augmentation/induction needed
541
Q

what are the different types of operative vaginal delivery

A

forceps, ventouse

542
Q

what are the indications for forceps/ventouse delivery

A
  • failure to progress to second stage
  • foetal distress in second stage
  • maternal reasons e.g. tired
543
Q

what are the prerequisistes for forceps/ventouse delivery

A

full diltatation
cephalic presentation
presenting part engaged

544
Q

what are the complications of forceps/ventouse delivery

A
  • failure
  • maternal/foetal trauma
  • postpartum haemorrhage
  • urinary retention
545
Q

list the risks of c section

A
  • anaesthetic risks
  • infection
  • bleeding, may reuqire transfusion
  • vte
  • accidentally cutting baby
  • damage to surrounding tissues (needs cath)
546
Q

what are the indications for c section

A
  • failure to progress
  • foetal distress
  • maternal reasons
  • malpresentation/malposition
  • failed instrument delivery
547
Q

what is the definition of shoulder dystocia

A

inability to deliver shoulder after delivery of head

anterior shoulder does not enter pelvic inlet

548
Q

what are the complications of shoulder dystocia

A

foetal asphyxia
foetal death
birth trauma e.g. erb’s palsy, fractures (esp. clavicle)
maternal trauma

549
Q

which pregnancies are at risk of shoulder dystocia

A

macrosmoic foetus
foetus of diabetes mother
rotational instrumental delivery

550
Q

what is the management of shoulder dystocia

A
  • episiotomy
  • mcroberts position with suprapubic pressure
  • other obstetric manoeuvres
  • symphisiotomy last resort
551
Q

what are the different modes for intrapartum foetal monitoring

A
  • fhr
  • ctg
  • foetal blood sampling (tests ph and lactate)
552
Q

list the different types of intrapartum analgesia

A
  • entonox
  • im opiates (pethidine)
  • remifentanil pca
  • epidural
  • combined spinal-epidural
  • local
553
Q

what is the success rate for epidural in labour

A

95%

554
Q

what are the side effects of epidurals in labour

A 
dizziness, transient hypotension
dural tap (accidentally going through dura), causing headache
555
Q

what is the bishop score in labour

A

quantifies ripeness of cervix, station, effacement, dilatation, position of uterus

556
Q

how is foetal station evaluated in labour

A

compare head of foetus to position of ischial spines (pelvic inlet)
0 = at ischial spines, with range of -3 to +3 (from far away from ischial spines to degree of how much the head is past the ischial spines)

557
Q

what is the definition of cord prolapse

A

umbilical cord descends below presenting part when the membranes have ruptured.

558
Q

what happens with untreated cord prolapse

A

cord becomes compressed or goes into spasm, causing foetus to rapidly become hypoxic

559
Q

what are the risk factors for cord prolapse

A
  • preterm labour
  • preterm rupture of membranes
  • breech
  • polyhydramnios
  • abnormal lie
  • twin pregnancy
560
Q

how is cord prolapse diagnosed

A

cord palpated pv, or seen in introitus

fhr reduced, abnormal

561
Q

how is cord prolapse managed

A

the presenting part may be pushed back in to prevent compression of cord
tocolytics such as terbutaline
emergnecy c section

562
Q

what is the definition of uterine rupture

A

uterus tears de novo/old scar ruptures, causing haemorrhage

563
Q

how may uterine rupture present

A

constant lower abdo pain, pv bleeding
cessation of contractions
maternal collapse
fhr abnormalities

564
Q

what are the risk factors for uterine rupture

A

labour with scarred uterus (previous c section)

congenital uterine abnormalities

565
Q

how is uterine rupture prevented

A

avoid induction
caution when using oxytocin in women with previous c sections
elective c section for woemn with scars not in the lower segment

566
Q

what is the management of uterine rupture

A

maternal resus with iv fluids and blood
blood taken for clotting, hb and x match
urgent laparotomy for delivery, repair, stop bleeding
hysterectomy in some cases

567
Q

why is ctpa avoided in pregnancies with ?pe

A

xrays affect foetus

v/q instead

568
Q

define the peuperium

A

6 week period following delivery, when the body returns to its prepregnant state

569
Q

what is lochia

A

discharge from uterus in the peuperium - can be blood stained at first, but after that is white

570
Q

explain general postnatal care for women

A

mother and baby should not be separated
early mobilisation
pelvic floor exercises
counselling and practical help with breastfeeding
daily check for uterine involution, temp, hr, bp, perineal/c section wound check
advice regarding contraception
mental health

571
Q

what is the advice for contraception postnatally

A

usually started 4 weeks post delivery
cocp ci in breastfeeding due to inhibiting mild production
pop or iud (once screened for infection)

572
Q

which hormones is lactation dependent on

A

prolactin and oxytocin

oestrogen and progesterone inhibit prolactin

573
Q

what is the definition of primary post partum haemorrhage

A

over 500 ml blood loss within 24 hours of delivery or over 1000 ml after c section

574
Q

what are the causes for pph

A

4 t’s

1) tone - uterine atony
2) trauma - injury to birth canal e.g. perineal tear, vaginal tear etc
3) tissue - retention from placenta or foetus
4) thrombin: bleeding disorder/coagulopathy/dic

575
Q

how may pph be prevented

A

routine use of oxytocin in 3rd stage of labour or ergometrine, or both in combination to help contract the uterus

576
Q

what are the side effects of ergometrine

A

headaches, vomiting

577
Q

what is the management of primary pph

A 
resus, lie flat, iv access
get senior help
x match 6 units
volume restoration
manual removal of placenta if delayed explusion
pv to look for uterine inversion
iv oxytocin/ergometrine
bimanual compression of uterus
myometrium prostaglandin  injection
surgery, balloon tamponade, brace suture
hysterectomy
578
Q

what is the definition of secondary pph

A

excessive blood loss between 24 hours and 6 weeks postpartum

579
Q

what are the causes of secondary pph

A

endometritis +/- retained placental tissue

incidental gynae pathology or gestational trophoblastic disease

580
Q

what are the investigations for secondary pph

A

bloods: fbc, clotting, U+E, Xmatch
vaginal swab
uss - though hard to differentiate between clots and retained placental tissues

581
Q

what is the management of secondary pph

A

antibiotics
erpc may be required
histological examination for tissues for ?trophoblastic disease

582
Q

what is the definition of postpartum pyrexia

A

temp > 38 deg in the first 2 weeks pp

583
Q

what is the management of postpartum pyrexia

A

prophylactic antibiotics given to reduce the risk of sepsis
blood, urine, foetal, vaginal cultures taken
swabs for important pathogens e.g. group a strep, e coli, staph

584
Q

what are the most common causes of postpartum pyrexia

A

uti, chest infection, mastitis, perineal and wound infection

585
Q

does dvt cause pyrexia

A

yes - low grade

586
Q

in which women is pnd more common

A

socially and emotionally isolated
previous history
pregnancy complications

587
Q

what is the management of mental health problems in pregnancy/pp

A

drug review ideally preconceptually
risk assessment
if high risk, antidepressants continued in pregnancy
ssri’s preferred to fluoxetine
psychiatric review before delivery if hx of mental health problems

588
Q

what is peuperal psychosis

A

abrupt onset of psychotic symptoms, leading to psychiatric admission and drug therapy

589
Q

what are some of the medical problems that can result postpartum

A
  • dvt
  • hypertensiive complications take 24 hours to resolve
  • urinary retention
  • utis
  • incontinence
  • perineal trauma
  • bowel problems e.g. constipation, haemorrhoids
590
Q

list the complications of pph

A
  • hypovolaemic shock
  • dic
  • renal failure
  • liver failure
  • ards
591
Q

describe dic

A

widespread activation and consumption of clotting factors

592
Q

what is the management of dic

A

transfuse platelets, plasma,
ffp, ptcc, cryoprecipitate
protein c

593
Q

how is dic investigated

A

pt
aptt
platelet counts
fibrinogen levels

594
Q

what are the neuro conditions associated with prematurity

A
  • aponea of prematurity
  • hypoxic ischaemic encephalopathy
  • retinopathy
  • developmental disability
  • brain damage
595
Q

what are the cardioresp complications of prematurity

A

pda

rds

596
Q

what are the gi complications of prematurity

A

hypoglycaemia

nec

597
Q

what are the haem complications of prematurity

A

anaemia of prematurity
hyperbilirubinaemia
thrombocytopenia

598
Q

what are the infective complications of prematurity

A

due to underdeveloped immune system: sepsis, uti’s, pneumonias

599
Q

list the steps in examining a post partum woman

A

1) palpate abdomen, examine scars
2) bp
3) pv: tears, bleeding, episotomy, incontinence
4) smear in some
5) weight
6) hb, glucose tolerance in past gestational diabetes
7) breast examination

600
Q

what is the management of mastitis

A
  • rest, analgesia, fluids, massage
  • warm cloth compress
  • express milk
  • abx if likely due to infection (flucloxacillin for staph)
601
Q

list the different degrees of perineal tear

A 
1st = fourchette
2nd = perineum
3rd = anal sphincter
4th = anal mucosa torn
602
Q

what is a partogram

A

chart used to record progress of dilatation of the cervix, plotted against time

603
Q

what is the treatment for neonatal group b strep infection

A

iv penicillin

604
Q

what does meconium aspiration cause in the newborn

A

severe pneumonitis

605
Q

what are the different signs/symtpoms that indicate foetal distress

A

ph <7.2 in foetal scalp blood sample
meconium stained amniotic fluid
fhr abnormal when auscultated with hand held doppler
ctg abnormalities detected

606
Q

what is the drcbravado abbreviation for ctg

A 
dr = define risk
c = contractions (less or more than expected)
br = baseline rate
v = variability
a = acceleration
d = deceleration
o = overall assessment
607
Q

what should normal ctg baseline rate be, and what can cause it to be increased

A

110-160

infection, fever, hypoxia

608
Q

list the steps in diagnosing foetal distress

A
  • fhr -> abnormal, meconium, high risk
  • ctg -> abnormal
  • fbs -> abnormal
  • delivery by quickest route
609
Q

what are the contraindications for epidural

A 
sepsis
coagulopathy/anticoagulant use
neuro disease
spinal abnormalities
hypovolaemia
610
Q

what is assessed when a woman presents in labour, after taking hx and obs

A

pv examination to check cervical effacement - cofnirms labour
degree of descent assessed
colour of any leaking liqour assessed
fhr, ctg

611
Q

what is considered slow progress of labour

A

cervical dilatation at rate of less than 1cm per hour after latent phase

612
Q

how long do doctors usually wait for the cervix to fully dilate before putting lady in for c section

A

12 hours

613
Q

what is the problem with epidurals and labour

A

woman may not feel contractions so are encouraged to contract 3 times for 10 seconds each time. if after 1 hour delivery not imminent -> instrumental/c section

614
Q

how is the placenta examined once it is delivered

A

check the cord - 2 arteries and vein
check cotyledons if ant missing
the amniotic sac is examined

615
Q

what are the indications for induction of labour

A 
prolonged pregnancy
iugr
compromise
aph
prom
maternofoetal indications e.g. preeclapmsia
616
Q

what are the absolute contraindications for induction of labour

A

acute foetal compromise
abnormal lie
placenta praevia
pelvic obstruction - causing cephalopelvic disproportion

617
Q

what are the complications of induction of labour

A 
unsuccessful
risk of instrumental delivery/c section
overactivity of uterus-hypercontractility
aph/pph
pp infection
618
Q

list some of the physiological changes in pregnancy to the cardiovascular system

A
  • increased hb mass
  • increased plasma volume
  • fall in hb in 2nd trimester
  • physiological anaeamia of pregnancy
  • mild increase in wcc
  • fall in platelet count
619
Q

what hb level is considered anaemia in pregnancy

A

less than 104 g/L

620
Q

what ar ethe different types of aneamia in pregnancy

A
  • physiological
  • iron deficiency
  • folate deficiency
  • b12 deficiency
  • haemoglobinpathies
  • chronic disease, drugs etc
621
Q

what are the causes of iron deficiency anaemia in pregnancy

A
  • increased red cell mass
  • foetus and placenta demand
  • increased basal maternal requirements
  • blood loss at delivery
622
Q

what should be avoided with iron supplements

A
  • bran, oats, rye, fibre
  • tannins in tea
  • some veg
  • dietary calcium content increase
623
Q

list some of the causes for folate deficiency

A
  • malabsorption
  • haemolysis
  • haemoglobinopathies
  • myeloproliferative disease
  • anticonvulsants
624
Q

why are d-dimers not useful in ?pe for in pregnancy

A

raised in pregnancy anyway

625
Q

describe the concept of rhesus alloimmunisation

A

if mother rhesus negative and baby rhesus positive, mother can become exposed to the RhD antigen during pregnancy after release of foetal cells into maternal circulation. mother therefore produces IgM antibodies against RhD which do not cross placenta, however on reexposure to RhD (usually subsequent pregnancy), the mothe rproduces IgG antibodies against RhD which can cross placenta and cause haemolysis of foetal blood

626
Q

list some sensitising events for rhesus alloimmune reaction

A
  • threatened miscarriage
  • abdo trauma
  • cvs, amniocentesis, ecv
  • antepartum haemorrhage
  • delivery
  • blood trasnfusions
  • some sensitisation throughout normal pregnancy
627
Q

what is the main haemoglobin type in foetuses, found in minute quantities in adults

A

HbF (2 alpha and 2 gamma chains)

628
Q

what is the pathophysiology of sickle cell disease

A

single base change glutamic acid -> valine

HbS causes sickling and shape changes

629
Q

how are babies with haemolytic disease monitored and treated

A

ab levels
mca doppler uss
iv transfusion
exchange/topup transfusion after delivery

630
Q

how is sickle cell diagnosed

A
  • hb low
  • sickle cells on film
  • howell jolly bodies
  • nrbc
  • sickle solubility test/electrophoresis
631
Q

how can sickle cell disease affect pregnancy

A
  • mother: reduced hb, infection, crises increased

- foetus: miscarriage, iugr, stillbirth, prematurity

632
Q

what is the pathophysiology of thalassaemia

A

heterogenous group of disorders where there is reduced rate of synthesis of alpha or beta globin chains

633
Q

what are the clinical features of thalassaemia

A

severe anaemia
hepatospleomegaly
bm hyperplasia

634
Q

what is the treatment for thalassaemia

A

regular blood transfusions

folic acid, iron, vit c, splenectomy

635
Q

what is the process of ideintifying women at increased risk of having baby with haemoglobinopathies

A
  • booking visists and bloods
  • partner testing
  • increased risk couple is identified and counselled

Obs & Gynae (1 decks)

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