Obs and Gynae Flashcards
What is the mechanism of action of mifepristone?
It inhibits the progestational hormones, the progestins, resulting in the abortion of a pregnancy
What are the different types of morbidly adherent placenta?
Morbidly adherent placenta (too deep):
Acreta – superficial myometrium
Increta – deeper myometrium
Percreta – into other abdominal organs
Which is the only immunoglobulin to cross the placenta?
only Ig to cross placenta
role in Rhesus disease/haemolytic disease of the new born?
IgA - Secreted
breast milk
IgD – B-cell membranes
no know effector function as serum protein
IgE – mast cells
anaphylaxis
IgG - different sub-types (1-4);
only Ig to cross placenta
role in Rhesus disease/haemolytic disease of the new born?
IgM – pentameric structure
“early” antibody
role in Rhesus disease/haemolytic disease of the new born?
What is the Aetiology for Rhesus disease (haemolytic disease of the new born)?
Rh-ve mother (dd) X Rh+ve father (DD or Dd)
50% to 100% offspring affected
There is sensitization in the first pregnancy (IgM)
In subsequent Pregnancy there is a rapid immune response (IgG)
Lysis of fetal RBCs
Fetal aneamia…
Fetal death?
Haemolytic disease of the new born: Maternal Ig raised against Paternal antigens on fetal red blood cells A, B,O and Rhesus-C, -D or -E Most common Rhesus-D Prevalence – 15% in Caucasians Lower in other ethnicities Very uncommon in Orientals
What is the treatment for Rhesus disease (haemolytic disease of the new born)?
Anti-D which is Anti-Rh+ve IgG - It stops fetal RBCs from being attacked.
Prophylactic anti-D given as intra-muscular injection
Usually within 72 hrs of exposre to fetal RBCs
Dose – gestation-dependant
First trimester:
very small vol fetal blood
Sensitization unlikely
“standard” dose anti-D given
Second/third trimester:
greater feto-maternal transfusion (several mls)
Sensitization likely
Larger dose anti-D given
Kleihauer test performed
Test maternal blood to determine proportion of fetal cells present
Relies on fetal cells resisting alcohol/acid denaturation
What are the negative sequlae of gestational diabetes in the baby and mother?
Poor glycaemic control results in a macrosomic infant (birth weight >5Kg). The Infant is at increased risk of:
Traumatic delivery – too big for the hole!
Shoulder dystocia
Still birth
Congenital malformation – cleft palate most common
Mother is at increased risk of: Ketoacidosis Pre-eclampsia Coronary heart disease Nephropathy Etc.
Select the single best answer which describes the Major Histocompatibility Molecule exclusively expressed on the extra-villus trophoblast.
1) HLA-A
2) HLA-B
3) HLA-G
4) HLA-H
5) HLA-I
HLA-G
HLA-C ,HLA-E also expressed
The syncitiotrophoblast does not activate the maternal immune system. Select the single best answer which describes why this occurs.
1) The syncitiotrophoblast expresses maternal antigens and is therefore seen as “self” by the maternal immune system.
2) The syncitiotrophoblast expresses modified paternal antigens and is therefore seen as “self” by the maternal immune system.
3) The syncitiotrophoblast does not express any “self:non-self” antigens and so does not stimulate the maternal immune system.
4) The syncitiotrophoblast expresses fetal antigens and is therefore seen as “self” by the maternal immune system.
5) The syncitiotrophoblast expresses paternal antigens and is therefore seen as “self” by the maternal immune system.
3) The syncitiotrophoblast does not express any “self:non-self” antigens and so does not stimulate the maternal immune system.
Select the single best answer which describes a drug which inhibits uterine contractions by antagonising the action of oxytocin.
1) Atosiban
2) Carboprost
3) Misoprostol
4) Nifedipine
5) Ritodrine
1) Atosiban
Select the single best answer which describes a drug which induces uterine contraction by stimulation of alpha 2 adrenergic receptors.
1) Atosiban
2) Ergometrine
3) Misoprostol
4) Ondansatron
5) Salbutamol
2) Ergometrine
What is the role of human Chorionic Gonadotrophin (hCG) in pregnancy?
Blastocyst hCG secretion prevents regression of the corpus luteum which synthesises progestins until placenta forms.
Around day 6-7 Post-Fertilisation, Trophoblast cells of blastocyst secrete human chorionic gonadotrophin (hCG).
Progestins:
“Pro-gestational” hormones; essential for successful pregnancy
Prepares endometrium and uterus for implantation
Proliferation, vascularisation and differentiation of endometrial stroma
Promotes myometrial quiescence
represses pro-contractile proteins (Gap junctions)
impairs oxytocin and PGF2a synthesis
Increases maternal ventilation
Promotes glucose deposition in fat stores
What is the role of Oestrogen in prenancy?
Oestrogens:
Oestrone (E1), 17b-Oestradiol (E2), Oestriol (E3)
Source – ovary initially. Later in pregnancy variable – both fetal and maternally derived from androgenic precursors
Promotes changes in cardiovascular system
Alters carbohydrate metabolism – insulin resistance?
E3 main oestrogen in pregnancy
Indicator of fetal wellbeing; decline correlates with fetal distress
E2 signals endometrial epithelium proliferation/differentiation
Facilitates progesterone action by increasing number of endometrial progesterone receptors
How is breast cancer diagnosed?
Triple Assessment:
• Clinical score 1-5
• Imaging score 1-5 (Mammography/ultra sound)
• Biopsy score 1-5 (core biopsy)
What are the signs and symptoms of breast cancer?
Presenting Symptoms: • Painless lump • Nipple discharge • Nipple in-drawing • Pain and tenderness NOT a common feature
Presenting signs: • Painless Lump. • Irregular • Hard • Fixed • Skin tethering. • Indrawn nipple.
What are the receptor sub types for breast cancer?
oestrogen
progesterone
HER2
What do you look for when assessing a CTG?
Dr = Define risk
C = Contractions
Bra = Baseline rate
V = Variability
A = Accelerations
D = Decelerations
Early decelerations
Variable decelerations
Late decelerations
O = OverallWhat are the normal parameters for CTG?
Baseline rate: 110-160 BPM
Variability: >5 BPM
Accelerations: Present
Decelerations: Early decelerations
What are the parameters for an abnormal CTG?
Baseline rate: <100bpm >180bpm
Variability: <5 BPM >90mins
Accelerations:
Decelerations: late decelerations
What is menopause?
Cessation of menstruation
Average age 51 years
Diagnosed after 12 months of amenorrhoea
Onset of symptoms if hysterectomy
What is perimeopause?
Period leading up to the menopause
Characterised by irregular periods and symptoms eg hot flushes, mood swings, urogenital atrophy
If >45 years, do not measure FSH for diagnosis
Vasomotor symptoms
experienced by 60-80% women
last on average 2-7 years
Impact on sleep, mood and QoL
Generalise symptoms mood change/irritability loss of memory/concentration headaches, dry and itchy skin, joint pains loss of confidence, lack of energy
What are the long term symptoms of the manopause?
Osteoporosis:
Menopause well established as a significant risk factor
Effects reliably reversible with oestrogens
Cardiovascular disease:
Adverse changes in lipid
Increased prevalence with early menopause
Dementia:
Increased prevalence with early menopause
What are the risks and benefits of HRT?
Benefits:
Relief of menopause symptoms
Bone mineral density protection
Possibly prevent long term morbidity
Risks: Breast cancer VTE Cardiovascular disease Stroke
Breast cancer risk:
Baseline risk varies from one woman to another
HRT with oestrogen alone – little or no change in risk
HRT with oestrogen + progesterone – increased risk
Increased risk is related to treatment duration and reduces after stopping HRT
What is the treatment procedure for HRT in women with breast cancer?
Discontinue HRT in women diagnosed with BC
Do not offer HRT routinely to women with menopausal symptoms and a history of breast cancer.
HRT may, in exceptional cases, be offered to women with severe menopausal symptoms and with whom the associated risks have been discussed
Which patients should recieve transdermal HRT?
Gastric upset eg Crohns Need for steady absorption eg migraine/epilepsy Perceived increased risk of VTE Older women ‘higher risk of HRT’ Medical conditions eg hypertension Patient choice
What is Premature Ovarian Insufficiency?
Menopause <40 yrs
Natural or Iatrogenic
Primary or secondary
Majority of cases – idiopathic
Other natural causes: Chromosome abnormalities FSH receptor gene polymorphisms Inhibin B mutations Enzyme deficiencies Autoimmune disease Iatrogenic Surgery Chemotherapy Radiotherapy
Diagnosis FSH >25IU/l – 2 samples >4 weeks apart + 4 months of amenorrhoea
What is the treatment for Premature Ovarian Insufficiency?
Mainstay of treatment is Estrogen replacement:
HRT
COCP (combined oral contraceptive pill)
Androgen replacement:
Testosterone gel
Fertility:
Donor egg
What is the grading for a urogenital prolapse?
First degree: Lowest part of prolapse halfway down vaginal axis at introitus
Second degree: Lowest part extends to introitus, through introitus on straining
Third degree: lowest part extends through introitus and outside vagina.
Procidentia: third degree uterine prolapse
Where is the perineal body and what is its function?
Lies between vagina and rectum
Point of insertion for muscles of pelvic floor
Name 3 antenatal screening programmes
Fetal Anomaly Screening Programme:
Down’s, Edward’s and Patau’s Syndrome Screening Programme
18+0 - 20+6 week anomaly scan
Infectious Diseases Screening Programme:
Hepatitis B
HIV
Syphilis
Sickle Cell and Thalassaemia Screening Programme
Name 2 newborn screening programmes
New-born blood spot screening programme: Cystic fibrosis (CF) Congenital hypothyroidism (CHT) Sickle cell disease (SCD) Inherited metabolic diseases (IMDs) x6
New-born hearing programme
New-born & 6 – 8 week infant physical examination screening programme
What are the 6 Inherited metabolic diseases (IMDs) that are tested for on the new-born blood spot screening programme?
phenylketonuria (PKU) medium-chain acyl-CoA dehydrogenase deficiency (MCADD) maple syrup urine disease (MSUD) isovaleric acidaemia (IVA) glutaric aciduria type 1 (GA1) homocystinuria (HCU)
What is Edward’s syndrome?
Trisomy 18
Babies with Edward’s syndrome have an extra copy of chromosome 18 in each cell
T18 affects about 3 of every 10,000 births
Incidence increases with maternal age
Most babies with Edward’s will die before they are born, be stillborn or die shortly after birth
All babies born with T18 will have a wide range of problems, which are usually extremely serious.
Babies affected by T18 can have heart problems, unusual head and facial features, major brain abnormalities and growth problems
What is Patau’s syndrome?
Trisomy 13
Babies with Patau’s syndrome have an extra copy of chromosome 13 in each cell
Incidence increases with maternal age
T13 affects about 2 of every 10 000 live births (3rd most common Trisomy)
Most babies with Patau’s will die before they are born, be stillborn or die shortly after birth
Associated with multiple severe fetal abnormalities:
80% have congenital heart defects
Holoprosencephaly (the brain doesn’t divide into two halves)
Midline facial defects
Abdominal wall defects
Urogenital malformations
Abnormalities of hands and feet
Pregnant women should be offered at least 2 ultrasound scans during pregnancy. When should theses scans take place and what is their purpose?
Early Ultrasound Scan usually between 10 to 14 weeks gestation used mainly for dating the pregnancy and confirming viability
Primarily to assess gestational age however will also reveal:
Fetal demise
Multiple pregnancy
May reveal :
Fetal abnormality i.e. anencephaly, exomphalus
Increased Nuchal Translucency
Ultrasound to screen for structural anomalies ideally between 18 weeks 0 days and 20 weeks 6 days gestation.
The second scan is designed:
to identify major abnormalities which indicate the baby may die shortly after birth
to identify conditions that may benefit from treatment before birth
to plan delivery in an appropriate hospital/centre
to optimise treatment after the baby is born
to provide choices for the woman and her family about continuance or termination of the pregnancy
The timing of the scans allows for further diagnostic tests if required and ensures women have time to consider decisions about continuing their pregnancy.
What are the components of the New-born & infant physical examination (NIPE) and when is it carried out?
General physical examination and specific examination to identify:
Eye problems – including congenital cataracts - 2-3 babies per 10,000
Congenital Heart Defects -1 in 200 babies require treatment
Developmental Dysplasia of the Hips - 1-2 per 1000 babies
Undescended testes - 1 in 100 baby boys
First examination within 72 hours of birth
Second examination by GP at 6-8 weeks
Referral pathways
Early treatment to improve health & prevent long term disability.
Failsafe system to account for each baby
What is considered infertility?
Failure to conceive after 1 year
Approx 15% (1:7) of couples
Up to 25% couples overall
What are the risks of increasing maternal age on pregnancy?
decreased fertility
increased risk of miscarriage
increased risk of chromosomal abnormalities
There is also Increased risks of: Hypertension Diabetes IUGR Operative delivery Thromboembolism Maternal death
Couples can be reffered for fertility treatment after 1 year. What are the criteria for early referral?
Female criteria:
Age > 35 Menstrual disorder Previous abdominal / pelvic surgery Previous PID / STD Abnormal pelvic examination
Male criteria:
Previous genital pathology Previous urogenital surgery Previous STD Systemic Illness Abnormal genital examination
What pre-conceptual advice would you give to a couple that are trying for a baby?
Intercourse – 2-3 x week Folic acid – 0.4mg (5mg high risk) Smear Rubella Smoking – cessation services Pre-existing medical conditions Drug history (prescribed / recreational) Environmental / occupational exposure Alcohol (women none) Weight (BMI 19 – 30)
What are the investigations of choice for infertility?
Initial investigations by GP:
Hormone profile (D2 FSH, D21 Prog) TFT, Prolactin – if indicated Rubella Smear Swabs Semen analysis
Ovulation / ovarian function Semen Quality Tubal Patency (+ Uterus)
How would you test for ovulation and ovarian reserve?
Ovulation: Mid-luteal phase (roughly day 23 of cycle) Progesterone <16 anovulation >16 < 30 equivocal > 30 ovular Series if long / irregular cycles
Ovarian reserve function
FSH
>8.9 - low response
<4 - high response
Antral Follicle Count (AFC)
<4 - low response
>16 - high response
Antimullerian Hormone (AMH)
<5.4 - low response
>25 - high response
What would be considered a normal result for semen analysis?
WHO (2010) methodology:
Count (>15 million/ml) Motility (>40%) Morphology (>4%) Total >39 million Repeat if abnormal Anti-sperm Antibodies – not required
Interpret semen analysis in light of history – illness, drugs etc
Further Analysis may be required if the result is abnormal. This may involve:
Clinical examination Secondary sexual characteristics Testicular size Further tests (if Count <5m/ml) Endocrine (FSH, LH, Test, Prolactin) Karyotype (e.g. Klinefelters) Cystic Fibrosis Screen – link with CBAVD Testicular biopsy (azoospermia) Only if cryopreservation facilities Imaging – Vasogram, ultrasound, Urology
how is Tubal Patency testing performed?
Low risk:
HysterSalpingoGram (HSG)
Hysterosonocontrast sonography (HyCoSy)
High risk: When pathology suspected: STI, PID Pain Previous surgery Perform a Laparoscopy with dye. Swabs must be taken before any instrumentation
What are the treatment options for male infertility?
Mild - Intrauterine Insemination (IUI) - ?
Moderate abnormality - IVF
Severe – Intracytoplasmic Sperm Injection (ICSI)
Azoospermia:
Surgical Sperm Recovery
Donor Insemination
Surgery:
Correction of epidymal block
Vasectomy reversal
Varicocele – no benefit
Hormonal:
Hypogonadotrophic hypogonadism - Gonadotrophins
Hyperprolacinaemia - Bromocriptine with sexual dysfunction
What are the criteria for PolyCystic Ovarian Syndrome (PCOS)?
Rotterdam Criteria 2003 - 2 out of 3 criteria
Anovulation / oligo/amenorhoea
Polycystic ovaries on scan (TVS):
One ovary
>12 small follicles
Vol > 10cc
Raised Androgens:
Clinical or biochemical
exclude adrenal cause)
What is the treatment for infertility in PCOS?
Normalise weight
Clomifene (or Tamoxifen): Up to 6 cycles (NICE 2013) Monitor (Progesterone & USS) Inform of multiple preg rate (6-8%) >12 months ? Ovarian Ca risk
Metformin: Less effective than clomifene alone Less effective in obese May help if clomifene resistant GI side effects
In Clomifene / metformin resistant PCOS the followinf can be used:
Laparoscopic Ovarian Drilling
Gonadotrophin OvuIation Induction
Name 3 causes of Tubal disease
Infections:
Chlamydia
Gonorrhoea
Endometriosis
Surgical:
Adhesions
Sterilisation
What is the class and mechanism of action of Clomiphene?
Clomifene is in the selective estrogen receptor modulator (SERM) family of medication.
Clomifene is a nonsteroidal SERM that inhibits estrogen receptors in the hypothalamus, inhibiting negative feedback of estrogen on gonadotropin release, leading to up-regulation of the hypothalamic–pituitary–gonadal axis. It works by causing the release of GnRH by the hypothalamus, and subsequently gonadotropin from the anterior pituitary. By competing with estrogen for binding sites at the hypothalamic level, the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), secretion is increased, which results in ovarian follicle maturation, followed by the preovulatory LH surge, ovulation, and the subsequent development of the corpus luteum.
Name 4 methods of assisted conception
Ovulation Induction (OI)
Stimulated Intrauterine Insemination (SIUI)
In Vitro Fertilisation (IVF): Intracytoplasmic Sperm Injection (ICSI) Surgical Sperm Recovery (PESA/TESE) Embryo Freezing Assisted Hatching Blastocyst Culture
Donor Insemination
Donor Egg
Donor Embryo
Host Surrogacy
What are the risks of IVF?
Multiple Pregnancy Miscarriage Ectopic Fetal abnormality? Ovarian Hyperstimulation Syndrome (OHSS) 1-5% Egg Collection (1:2000) Longer term - ? Ovarian Ca
What are the NICE criteria for IVF?
Treat after 2 years or 12 months insemination
Discuss risks and benefits
Full cycle of treatment includes freezing
Women < 40 years
3 full cycles
Stop once age = 40
Women 40-42
1 full cycle (if no previous IVF, no low ovarian reserve)
Cancelled cycles don’t count (unless low ovarian reserve)
Private cycles count against total
What are uterine fibroids?
Leiomyomas - benign tumours of myometrium
20% of women of reproductive age
Often asymptomatic
Well circumscribed whorls of smooth muscle cells with collagen
Single or multiple
Vary from microscopic growths to tumours that weigh as much as 40 kg
What are the pathological causes of Heavy Menstrual Bleeding (HMB)?
Uterine fibroids (20-30%) Uterine polyps (5-10%) Adenomyosis (5%) Endometriosis – rarely presents as HMB but identified in <5% of cases of Abnormal Uterine Bleeding
Gynaecological malignancy rarely presents as HMB but can present as prolonged Inter-Menstrual , Post Coital or Post-menopausal bleeding.
40-60% of women with HMB have no uterine, endocrine, haematological or infective pathology on investigations –DUB (Dysfunctional Uterine Bleeding) of ovulatory (regular cycle) or anovulatory (irregular cycle) type
What are Uterine Polyps?
common benign localised growths of the endometrium
fibrous tissue core covered by columnar epithelium
arise as a result of disordered cycles of apoptosis and regrowth of endometrium
malignant changes rare
What is Endometriosis?
endometrium type of tissue lying outside the endometrial cavity
usually lies within peritoneal cavity
Rarely in distal sites
like endometrium, responds to cyclical hormonal changes and it bleeds at menstruation
What is Adenomyosis?
ectopic endometrial tissue within the myometrium (muscle of the womb)
Localised - Adenomyoma
Diffuse
What is the NICE guidance for the investigation of Heavy Menstrual Bleeding?
FBC
Trans-Vaginal Scan
Endometrial biopsy if >45yrs and:
IMB
Unresponsive to treatment
Place of hysteroscopy:
Unresponsive to treatment
Abnormal scan - Diagnose polyps/define fibroids
Assess suitability for OP ablation
