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Phase 3a > Obs & Gynae > Flashcards

Obs & Gynae Flashcards

1
Q

Why do contact tracing?

A

-Prevent re-infection of index case
-Identity and treat asymptomatic infected individuals
Public health measures

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2
Q

What is the average age for menopause?

A

Average is 51- greater than or equal to 45 is considered normal range

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3
Q

What is considered abnormal menopause?

A

Younger than 40 years premature ovarian insufficiency

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4
Q

Why does HRT have progesterone as well as oestrogen?

A

Progesterone is needed to prevent over proliferation of the endometrium caused by oestrogen

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5
Q

What’s the difference between gestational HTN and preeclampsia?

A

Gestational HTN = new HTN after 20 weeks of gestation >140/90 with little or no proteinuria.

Preeclampsia = new HTN as above but with high levels of proteinuria. There may be associated swelling of hands, feet and face.

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6
Q

What’s the pathophysiology of preeclampsia?

A
  • vasoconstriction leading to HTN
  • platelet activation leading to intravascular coagulation
  • endothelial dysfunction i.e. fluid shifting from vascular to interstitial compartments
  • spiral arteries fail to be converted to vascular sinuses
  • causes placental ischemia
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7
Q

What are complications of pre-eclampsia?

A

Mum:

  • CVA
  • DIC
  • Liver failure
  • Renal failure

Bab:

  • growth retardation
  • early placental detachment
  • death
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8
Q

What is the metabolic state of pregnancy?

A

PO2 goes up
PCO2 goes down

Compensated metabolic alkalosis

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9
Q

What is the DDx for acute pelvic pain?

A 
Gynaecological 
-Endometriosis (ruptured endometrioma)
-Ovarian Cyst (rupture)
-Ovarian Torsion 
-Ectopic Pregnancy 
-PID
-Malignancy 
Non-Gynaecological 
-UTI
-Appendicitis
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10
Q

Define Acute Pelvic Pain.

A

Acute lower abdomen or pelvic pain that may be constant or intermittent that lasts for less than 3 months

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11
Q

Define Chronic pelvic pain.

A

Intermittent or constant pain felt with within the lower abdomen or pelvis that lasts for 6 months. It is not associated exclusively with menstruation, intercourse or pregnancy.

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12
Q

What test would you do for acute pelvic pain?

A
  • Urine - dipstick for signs of infection or kidney damage
  • Pregnancy test - HcG if +ve but no sign of pregnancy in uterus
  • Ultrasound
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13
Q

What is the DDx for Chronic Pelvic Pain?

A
  • Endometriosis
  • adenomyosis
  • PID
  • STI
  • Pregnancy
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14
Q

What sign on bimanual examination suggests PID or ectopic pregnancy?

A

Cervical motion tenderness (cervical excitation) - Woman finds cervix being touched more painful than usual examinations.

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15
Q

Define Normal labour.

A

Baby is born spontaneously in the vertex position between 37-42 weeks. Mother and baby are well.

-No medical intervention needed

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16
Q

What are the 3 stages of labour?

A

1 - Dilation period - latent (up to 4cm) and active (up to 10cm)
2 - Engagement/Expulsion period from complete dilation to complete delivery - cardinal movements of the foetus
3 - After birth period

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17
Q

Define Cervical Effacement.

A

Also known as cervical ripening - the cervix thins and moves up to become part of the uterine wall

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18
Q

What happens during the latent phase of labour?

A
  • irregular contractions
  • mucoid plug is passed through the vagina
  • cervix effaces
  • can take 6 hours - 2-3 days.
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19
Q

How does the second phase of labour differ for primiparous women and multiparous women?

A
  • longer in primip women

- 45-120mins vs 15-45mins

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20
Q

Why is delayed clamping of the umbilical cord recommended?

A

delay for 30 seconds helps to increase foetal haematocrit and decreased the need for transfusion.

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21
Q

Define engagement.

A

When the largest part of the babies head has entered the pelvis.

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22
Q

What is the process of movements does a foetus goes through when being birth?

A
  • descent down to the ischial spines
  • flexion head presses onto chest
  • internal rotation - foetal shoulders rotate
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23
Q

What happens during the 3rd stage of birth?

A
  • delivery of placenta and membranes + controlling of bleeding
  • routinely give syntometrine (oxytocin + ergometrine maleat) reduces third stage to <5 mins and reduces risk of post partum haemorrhage
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24
Q

What’s the difference between chronic hypertension, gestational HTN and preeclampsia?

A

Chronic HTN - diagnosed pre pregnancy or before week 20
Gestational HTN - increased BP after week 20
Preeclampsia - increased BP after week 20 + proteinuria

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25
Q

What are some systemic features of preeclmapsia?

A
  • headache
  • vision disturbance
  • RUQ pain - epigastric pain - hepatic ischaemia
  • reduced urine output
  • lower abdomen pain - placental abruption
  • pitting oedema
  • pulmonary oedema
  • stroke
  • eclampsia (essentially seizure)
  • hyperreflexia
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26
Q

What are risk factors for preeclampsia?

A
  • previous preeclampsia
  • FHx
  • Diabetes
  • Primagravida
  • Renal disease
  • obesity
  • connective tissue disease - RA/SLE
  • already having HTN
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27
Q

What is the pathophysiology of endometriosis?

A
  • condition where endometrial tissue grows outside of the uterus
  • relapsing and remitting as tissue responds to changing levels of hormones during menstrual cycle (therefore Sx cyclical)
  • Sampson’s theory - retrograde menstruation carries sloughed off endometrial cells that stick to none uterine sites and grow and thicken in accordance to menstrual cycles
  • endometrial patches are oestrogen dependent
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28
Q

What are the symptoms of Endometriosis?

A

1/3 asymptomatic

  • chronic pelvic pain - worsens before meneses
  • deep dyspareunia
  • dysmenorrhea
  • intermenstrual bleeding
  • infertility
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29
Q

What sites can endometriosis implants be found?

A
  • ovaries
  • fallopian tubes
  • cervix
  • bladder
  • less commonly - extra-pelvic organs (lungs or diaphragm)
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30
Q

How do you diagnose endometriosis?

A
  • patient history
  • physical examination - rectovaginal tenderness, adnexal masses
  • TVUS - evidence of chocolate cysts
  • confirmatory laparoscopy
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31
Q

How do you medically treat endometriosis?

A

first line - mild to moderate:
-NSAIDS + continuous hormone contraceptive

second line -severe:
-GnRH agonists - buserelin

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32
Q

How do you surgically treat endometriosis?

A

first line - laparoscopic excision and ablation of endometrial implants
second line - hysterectomy w/ or w/o bilateral salpingo-oophorectomy

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33
Q

Describe the pattern of pain seen in endometriosis?

A
  • cyclical pelvic pain
  • in a young woman
  • low parity
  • dyspareunia
  • dysmenorrhea
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34
Q

How does endometriosis effect fertility?

A
  • lowers fertility
  • immune factors
  • oocyte toxicity
  • adhesions
  • tubal dysfunction
  • ovarian dysfunction
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35
Q

What are the main epidemiological differences between adenomyosis and endometriosis?

A

endo - young and nulliparous

adeno - older and multiparous

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36
Q

Describe the pathophysiology of adenomyosis?

A
  • endometrial tissue and stroma extend into the uterine myometrium
  • causing diffusely enlarged and thickened myometrium
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37
Q

How does adenomyosis present?

A
  • cyclical pain
  • dysmenorrhea
  • dyspareunia
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38
Q

How do you treat adenomyosis?

A

-hormonal suppression or removal

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39
Q

How may a fibroid present?

A
  • asymptomatic
  • heavy periods
  • anaemia
  • infertility
  • miscarriage
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40
Q

How would you remove a fibroid whilst trying to preserve fertility?

A

myomectomy

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41
Q

If you suspect polyps, what must you also check for?

A

-histologically test for endometrial cancer because there’s a close association

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42
Q

Define primary and secondary amenorrhoea.

A

primary - failure to start menstruating (Ix at 16 w/ secondary sex characteristics or 14 w/o)
secondary - menstrual bleeding stops for over 6 months NOT due to pregnancy

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43
Q

What are some causes of primary amenorrhoea?

A

w/o secondary sex characteristics:

  • turner’s syndrome
  • congenital adrenal hyperplasia

WITH secondary sex characteristics:
-genitourinary malformation - imperforate hymen

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44
Q

What are some causes of secondary amenorrhoea?

A
  • HPA dysfunction - stress, exercise, low weight
  • hyperprolactinaemia - inhibits FSH & LH
  • PCOS
  • menopause
  • uterine adhesions
  • asherman’s syndrome
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45
Q

What investigations would you do for someone presenting with amenorrhoea?

A
  • beta HCG - rule out pregnancy
  • serum free androgens - raised LH and progesterone suggests PCOS
  • prolactin levels
  • TFTs
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46
Q

Test results show low FSH and low LH in a woman presenting with amenorrhoea. What are you differentials?

A
  • suggests dysfunction of the HPA axis
  • stress, exercise, low weight
  • hyperprolactinaemia
47
Q

Test results show high FSH and high LH in a woman presenting with amenorrhoea. what are you differentials?

A
  • suggests ovarian dysfunction
  • PCOS
  • menopause
48
Q

What do irregular periods, being every 3-4 months, tend to indicate?

A

oligomenorrhoea - indicates anovulation

49
Q

How do you treat PCOS?

A

NOT FOR FERTILITY Tx

  • lifestyle advice - lose weight
  • dianette - used for hirsutism + contraception

FERTILITY WANTED
-Clomiphene for ovulation induction

50
Q

What’s the difference between primary and secondary dysmenorrhoae?

A

primary = happens within 1-2 years of menarche, pain starts just before or within hours of onset of period, supra pubic cramps that may radiate

Secondary = develops many years after menarche and is the result of a different underlying pathology

51
Q

What is the first & second line treatment for primary dysmenorrhoea?

A

first = mefenamic acid (NSAID)

Second = COCP if not already on LARC

52
Q

What is the medical management of a uterine miscarriage?

A

Vaginal misoprostol (prostaglandin)

53
Q

What initial assessment would you do on a pregnant woman who is bleeding?

A
  • ABCD
  • abdo exam (if painful and tender more likely abruption than praevia)
  • TVUSS - diagnose praevia not abruption
  • maternal bloods - FBC, clotting, cross match
  • foetal heart rate with CTG
  • maternal BP
54
Q

What is the differential for a pregnant woman with antepartum haemorrhage?

A
  • placental abruption
  • placenta praevia
  • vasa praevia
  • low genital tracts causes (cervical polyps, vaginitis, vulval varioses)
55
Q

How does one manage an antepartum haemorrhage? what counselling would you offer further for the birth/future pregnancies?

A
  • offer corticosteroids (increased risk of prem bab)
  • serial USS for foetal growth (increased risk of poor growth)
  • C section - women with APH with associated maternal and/or foetal compromise should deliver immediately
  • increased risk of post partum haemorrhage so forewarn and be prepared
56
Q

What drug is given to shorten the length of the 3rd stage of pregnancy?

A

-IM syntocinon

57
Q

How do you immediately manage a post partum haemorrhage?

A
  • ABC
  • bloods - FBC, crossmatch
  • BP & HR
  • bimanual compression of the uterus
  • give oxytocin slowly
58
Q

What are the 4 Ts that can cause post partum haemorrhage?

A
  • Tone - uterine atony
  • Tissue - retained placenta
  • Tauma - lacerations//rupture
  • Thrombin - coagulopathy
59
Q

What are the increases risk of post partum haemorrhage?

A
  • macrosomia
  • placental abruption
  • placenta previa
  • multiple pregnancies
  • gestation HTN
  • prolonged labour
  • infection
  • obesity
  • induced labour
  • instrumental delivery
  • GA
  • coagulopathy
  • use of oxytocin in 3rd stage
60
Q

What surgical treatments are there for post partum haemorrhage?

A
  • Rush balloon catheter
  • artery ligation
  • haemostatic brace suture
  • hysterectomy
61
Q

define ovulation.

A

Ovarian follicle (oocyte + surrounding tissue) matures and ovulation occurs. The eff is ejected into the fallopian tubes & the surrounding tissue becomes the corpus luteum and produces progesterone and oestrogen.

62
Q

define fertilization.

A

Egg meets sperm and nuclei fuse forming a Zygote. Cells divide and form a blastocyst.

63
Q

What happens to the blastocyst in a normal pregnancy?

A

Implants into the uterus (day 5). Corpus luteum makes progesterone > oestrogen (necessary for implantation). Trophoblasts (outer blastocyst cells) burrow into the endometrium to form placenta. trophoblasts produce HCG from day 8 - tells corpus luteum there’s been successful implantation and needs to keep producing O&P.

64
Q

when is and what happens during the first trimester?

A
  • week 1 - 13.
  • Hormones are produced by the corpus luteum.
  • week 9 HCG peaks then falls - corpus luteum shrivels and placenta takes over.
65
Q

What cells produce pregnancy hormones during the 2nd & 3rd trimesters?

A
  • placental synctiotrophoblasts

- produce progesterone & estriol (type of oestrogen)

66
Q

What physiological changes happen during pregnancy?

A

CVS:

  • blood volume increases
  • plasma increases greater relative to haematocrit. (physiological anaemia of pregnancy)
  • HR increases
  • more blood through kidney = increase urinary frequency
  • uterus presses on pelvic veins = ankle oedema.

Resp:

  • Tidal volume increases (response to increase in progesterone loosening ligaments)
  • uterus presses on diaphragm = SOB

Gastro:

  • smooth muscle relaxation and decreased peristalsis = constipation and bloating
  • relaxation of the LOS - GORD

skin:
-Increase in melanocyte stimulating hormone = linea nigra and darkening areola

O&P:

  • breast development - increase blood flow = tingling, fullness and tenderness
  • O stimulates prolactin that causes milk production
  • O promotes blood clotting by increasing plasma fibrinogen and activity of coagulation factors - increased risk of VTE.
67
Q

A woman who’s 10 weeks pregnant presents to A&E with heavy vaginal bleeding. what are the potential DDx?

A
  • threatened miscarriage
  • missed/incomplete miscarriage
  • ectopic pregnancy
68
Q

What investigations would you perform for a suspected miscarriage?

A

-B HCG
-TVUSS:
~Os open?
~uterus size?
-Hx - have products of conception been seen?

69
Q

What are the features and management of a threatened miscarriage?

A
  • mild bleeding +/- pain
  • cervix closed
  • TVUSS - viable pregnancy

-management:
~if heavy bleeding admit/observe
~if not reassure and back to GP/midwife
~if greater than 12 weeks & rhesus -ve: give Anti-D

70
Q

What are the features & management of an inevitable miscarriage?

A
  • heavy bleeding
  • clots
  • pain
  • Cervix open
  • TVUSS - internal Os open

-management:
~if heavy bleeding admit + observe
~offer conservative/medical/surgical management
~if greater than 12 weeks & rhesus -ve: give Anti-D

71
Q

What are the features and management of a missed miscarriage?

A
  • asymptomatic or Hx of threatened miscarriage
  • on-going discharge
  • small dates for uterus
  • TVUSS - not foetal heart pulsation where crown is >7mm

-management:
~may want to rescan and second person confirmation
~manage conservatively/medically/surgically
~if greater than 12 weeks & rhesus -ve: give Anti-D

72
Q

What are the features and management of an incomplete miscarriage?

A
  • Products of conception partially expelled
  • Sx of missed miscarriage
  • may be so bleeding/clots
  • TVUSS - retained POC, proof that there was a previously an intrauterine pregnancy present.

-management:
~expectant, medical or surgical management
~if greater than 12 weeks & rhesus -ve: give Anti-D

73
Q

What are the features and management of an ectopic pregnancy?

A
  • acute onset iliac fossa or pelvic pain
  • amenorrhoea/missed period
  • vaginal bleeding
  • TVUSS - uterine pregnancy not visualised and have signs of ectopic (donut sign) on USS.

Management:
~medical or surgical management

74
Q

Define medical management of a miscarriage.

A
  • single dose of methotrexate given
  • prevents the proliferation of cytotrophoblasts and B-HVG secretion thus no progesterone support for pregnancy

-OR give vaginal misoprostol with pretreament of mifepristone 24hrs before hand

OR just vaginal misoprostol

OR oral misoprostol

GIVEN WHEN:

  • haemodynamically stable
  • no rupture
  • minimal abdo pain
  • no foetal heart
  • no presence of contraindicating disease i.e. renal, liver or active peptic ulcers.
75
Q

Define surgical management of a miscarriage.

A
  • laproscopic salpingectomy for ectopic
  • manual vacuum aspiration if <12 weeks
  • evacuation of retained products of conception under GA if >12 weeks.
76
Q

What are the risk factors for having an ectopic pregnancy?

A
  • previous ectopics
  • fallopian tube damage (previous surgery)
  • infertility - IVF, endometriosis, tubal disease
  • contraceptive failure - IUD, POP
  • Smoking
  • Age >35
  • STI - chlamydia
  • PID
  • submucosal fibroids
77
Q

Define small for dates.

A
  • A foetus who is small than the usual amount for the number of weeks gestation.
  • usually have birth weight <10th centile
78
Q

Define Large for Dates.

A
  • indication of high prenatal growth rate.

- usually have birth weights >90th percentile.

79
Q

Define a low birth weight.

A

<2500g

80
Q

Define foetal growth restriction.

A
  • pathological restriction of the genetic growth potential.

- babies may manifest evidence of foetal compromise - abnormal dopplers or reduced liquor volume

81
Q

Define foetal macrosomia.

A

Birth weight >4000g.

82
Q

What are the 3 main reasons for a Small for Dates foetus?

A
  • Normal - may happen because mother is small
  • non-placental mediated growth restriction
  • placental mediated growth restriction
83
Q

What are some causes of non-placental mediated growth restriction?

A
  • structural or chromosomal abnormalities of the foetus
  • inborn errors of metabolism
  • foetal infection
84
Q

What are some causes of placental mediated growth restriction?

A
  • placental abnormality - baby doesn’t get enough O2 and nutrients
  • decreased placental blood flow - HTN, DM, smoking, drug use)
  • placental abruption
  • placental praevia
  • maternal infection
85
Q

Define placental praevia.

A

placenta attaches fully or partially over the internal cervical os.

86
Q

What are some maternal risk factors for foetal growth restriction??

A

-low pre-pregnancy weight
-under nutrition during pregnancy
-substance misuse
-severe anaemia
-Chronic disease - HTN, CKD, DM, anti-phospholipid
-Smoking
-Age >40
-daily vigorous exercise
-Maternal SGA (small for gestational age)
-previous still birth
-TORCH infection:
~TOxoplasmosis
~Rubella
~Cmv
~Herpes

87
Q

What are some foetal risk factors for foetal growth restriction?

A
  • chromosomal abnormalities
  • congenital defects and dysmorphic syndromes
  • infection
88
Q

What are some placental risk factors for foetal growth restriction?

A
  • uterine fibroids
  • site of implantation - praevia or necreta
  • Antepartum haemorrhage
89
Q

How does the foetus adapt to reduction in placental perfusion and function?

A
  • movements become less as tries to conserve energy

- increased EPO to increase bloods capacity to carry oxygen - makes blood more viscous

90
Q

How is a diagnosis of foetal growth restriction made?

A

-foetal abdominal circumference or estimated foetal weight using USS

91
Q

Once foetal growth restriction is confirmed what further investigations would you perform?

A
  • ask about movements
  • urinanalysis
  • USS
  • uterine + umbilical artery doppler to assess blood flow
  • Karyotyping in sever cases
  • serological screening for TORCH infection
  • Surveillance of foetus using umbilical artery doppler
  • CTG
92
Q

How would you manage an SGA foetus?

A

prevention:

  • antiplatelet therapy with low dose aspirin in women high risk of preeclampsia
  • antenatal corticosteroids 25-36 weeks where delivery is being considered

Delivery:

  • C section if abnormal doppler
  • if normal, can be induced
  • closely monitor - foetus cannot handle periods of hypoxia

Post Partum:

  • Early feeding
  • keep baby warm
  • high risk of neonatal jaundice
93
Q

What does a low amniotic fluid index (AFI) suggest?

A

fluid volume = foetal urine output = kidney perfusion = placental function I.e. how much blood is getting to the foetus

94
Q

What is the difference between symmetrical and asymmetrical intrauterine growth restriction?

A
  • Symmetrical implies the body and head are in proportion so has been developing slowly from an early stages. More likely to be a central problem with the foetus and more likely to have neurological conditions when born.
  • Asymmetrical weight is restricted but head size is normal (spared). Foetus is undernourished and directs nutrients to the head. More likely to be a problem with the placenta.
95
Q

What are some risk factors for Macrosomia?

A
  • Maternal DM
  • maternal obesity
  • maternal excessive weight gain during pregnancy
  • previous macrosomia in other pregnancies
  • overdue pregnancy
96
Q

Describe the foetal response to maternal DM.

A
  • foetus stores extra glucose as fat.
  • foetal hyperinsulinaemia in response to high circulating blood glucose.
  • once baby is born is at a higher risk of hypoglycaemia
  • infant more likely to develop DM as a child
97
Q

What are the risk factors for breast cancer?

A
  • HRT
  • Post menopausal obesity
  • OCP
  • alcohol intake
  • multiple late pregnancy
98
Q

What are the potent breast cancer causing genes?

A
  • BRCA1
  • BRAC2
  • HER1
99
Q

What are the symptomatic features of breast cancer?

A
  • nipple inversion
  • orange peel skin
  • nipple discharge
  • pathological fracture
100
Q

How do you diagnose breast cancer?

A

Triple assessment

  • examination
  • imaging
  • histology
101
Q

Describe a breast cancer lump.

A
  • Hard
  • Irregular
  • fixed
102
Q

When would you use an MRI scan for breast screening?

A
  • high risk BRCA patient
  • younger women
  • women with implants
103
Q

What indications are there for mastectomy?

A
  • BRCA carriers
  • multiple tumours
  • personal choice
  • large tumours
104
Q

What is the most important prognostic factor for breast cancer?

A

-lymph node disease

105
Q

How do you identify lymph nodes affected by cancer?

A

Sentinel node lymph biopsy
Inject radioisotope into tumour and indentify node with gieger counter in surgery and take a couple for histological evaluation

106
Q

How are breast cancers graded?

A

1-3
1 good 3 bad
Varying levels of mitotic division on histo

107
Q

How do you decide which intermediate cancers are worse than others? And who to treat?

A
  • oncotype DX

- tests 21 different genes and allows for prognostication

108
Q

What adjunct therapies for breast cancer have caused an increase in survival rates?

A
  • endocrine tx - tamoxifen for oestrogen receptor sensitive cancers
  • radiotherapy
  • chemotherapy
  • trastuzumab - all her-2 positive disease
  • bisphosphonates - for post menopausal women and ER +ve women - reduces risk of bone Mets
109
Q

How does tamoxifen work?

A

Inhibits oestrogen receptors on breast cancer cells increases survival by 15-25%

110
Q

Why are herceptin breast cancers worse than none herceptin?

A

50% metastasize to the brain

111
Q

When do you give an aromatase inhibitor? How does it work?

A
  • post menopausal women with ER +ve cancer

- inhibits production of oestrogen

112
Q

How do you treat preeclampsia?

A
  • oral labetalol aiming for a BP less than 160/110.
  • nifedipine or hydralazine may be used
  • delivery is the most definitive Tx but depends on the clinical picture
113
Q

What’s the treatment for PID?

A

IM ceftriaxone + PO doxycycline + PO metronidazole

Phase 3a (15 decks)

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