Obs and Gynae Flashcards

1
Q

What is the mechanism of action of mifepristone?

A

It inhibits the progestational hormones, the progestins, resulting in the abortion of a pregnancy

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2
Q

What are the different types of morbidly adherent placenta?

A

Morbidly adherent placenta (too deep):
Acreta – superficial myometrium
Increta – deeper myometrium
Percreta – into other abdominal organs

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3
Q

Which is the only immunoglobulin to cross the placenta?

A

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?

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4
Q

What is the Aetiology for Rhesus disease (haemolytic disease of the new born)?

A

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
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5
Q

What is the treatment for Rhesus disease (haemolytic disease of the new born)?

A

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

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6
Q

What are the negative sequlae of gestational diabetes in the baby and mother?

A

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.
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7
Q

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

A

HLA-G

HLA-C ,HLA-E also expressed

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8
Q

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.

A

3) The syncitiotrophoblast does not express any “self:non-self” antigens and so does not stimulate the maternal immune system.

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9
Q

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

A

1) Atosiban

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10
Q

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

A

2) Ergometrine

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11
Q

What is the role of human Chorionic Gonadotrophin (hCG) in pregnancy?

A

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

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12
Q

What is the role of Oestrogen in prenancy?

A

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

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13
Q

How is breast cancer diagnosed?

A

Triple Assessment:
• Clinical score 1-5
• Imaging score 1-5 (Mammography/ultra sound)
• Biopsy score 1-5 (core biopsy)

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14
Q

What are the signs and symptoms of breast cancer?

A
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.
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15
Q

What are the receptor sub types for breast cancer?

A

oestrogen
progesterone
HER2

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16
Q

What do you look for when assessing a CTG?

A
Dr    = Define risk
C     = Contractions
Bra = Baseline rate
V     =  Variability
A     =  Accelerations
D     = Decelerations
         Early decelerations
         Variable decelerations
          Late decelerations
O    = Overall
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17
Q

What are the normal parameters for CTG?

A

Baseline rate: 110-160 BPM
Variability: >5 BPM
Accelerations: Present
Decelerations: Early decelerations

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18
Q

What are the parameters for an abnormal CTG?

A

Baseline rate: <100bpm >180bpm
Variability: <5 BPM >90mins
Accelerations:
Decelerations: late decelerations

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19
Q

What is menopause?

A

Cessation of menstruation
Average age 51 years
Diagnosed after 12 months of amenorrhoea
Onset of symptoms if hysterectomy

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20
Q

What is perimeopause?

A

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
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21
Q

What are the long term symptoms of the manopause?

A

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

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22
Q

What are the risks and benefits of HRT?

A

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

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23
Q

What is the treatment procedure for HRT in women with breast cancer?

A

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

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24
Q

Which patients should recieve transdermal HRT?

A
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
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25
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
26
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
27
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
28
Where is the perineal body and what is its function?
Lies between vagina and rectum Point of insertion for muscles of pelvic floor
29
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
30
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
31
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) ```
32
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
33
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
34
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.
35
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
36
What is considered infertility?
Failure to conceive after 1 year Approx 15% (1:7) of couples Up to 25% couples overall
37
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 ```
38
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 ```
39
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) ```
40
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) ```
41
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
42
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 ```
43
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 ```
44
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
45
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)
46
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
47
Name 3 causes of Tubal disease
Infections: Chlamydia Gonorrhoea Endometriosis Surgical: Adhesions Sterilisation
48
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.
49
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
50
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 ```
51
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
52
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
53
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
54
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
55
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
56
What is Adenomyosis?
ectopic endometrial tissue within the myometrium (muscle of the womb) Localised - Adenomyoma Diffuse
57
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
58
How would you treat Heavy Menstrual Bleeding?
Reassurance: Patient expectations of consultation Cohort study (14/17) suggests role Antifibrinolytics (Tranexamic acid): Inhibits tissue plasminogen activator 50% reduction in MBL Thrombotic events minimal NSAIDs (Mefenamic acid): Inhibits cyclooxygenase & block PGE2 receptors 25% reduction in MBL (in proportion to initial loss) Useful if dysmenorrhoea a symptom Progestagens: Least effective if used in the luteal phase Must be used from day 5 - 25 Best for anovulatory and chaotic bleeding MPA and NET equally effective Danazol: Inhibits sex steroid production, blocks receptors 86% reduction MBL (200mg) Limited by SE profile Combined oral contraceptive pill (COCP): Inhibits ovarian function 43% reduction in MBL Patient preference scores high ``` LNG IUS (MIRENA): Local release of levonorgestrel (20mcg) 85% reduction MBL at 3 months Significant drop out rate (20%) SE relate to progesterone and heavy IMB ``` Endometrial ablations: laser, electrosurgery, and balloons 85% patient satisfaction Day case procedure with fast recovery (two weeks) Complications related to procedure (perforation, fluid overload, intra-abdominal trauma) Myomectomy/Resection of Fibroids Hysterectomy: Vaginal, abdominal, LAVH, TLH 85% patient satisfaction Longer recovery (six weeks to three months) Complications related to procedure (bleeding, ureteric damage, intra-abdominal trauma)
59
What are the Indications and contraindications for Endometrial Ablation in Heavy Menstrual Bleeding?
``` Indications: Heavy menstrual loss Not expecting amenorrhoea Normal endometrium Uterus less than 12 weeks size Completed family ``` ``` Contrindications: Malignancy Acute PID Desire for future pregnancy Excessive cavity length ```
60
What are the side effects of the combined oral contraceptive pill?
``` OESTROGENIC (similar to pregnancy) Breast tenderness Nausea Headaches – Exclude migraine. Vaginal discharge ``` PROGESTOGENIC Acne, hirsutism Mood swings, low mood Breakthrough bleeding – Exclude other causes.
61
State 5 contraindications to Combined hormonal contraception.
``` All CHC contraindicated (UKMEC 3/4) in:- Migraine with aura Venous thromboembolism Hypertension BMI>35 Breast cancer Ischaemic heart disease Stroke Smoker >35 years ``` Protective against ovarian, endometrial and colon cancer Small increased risk of breast cancer (Cancer August 2014)
62
What cells make up the primordial follicles and what do they secrete?
granulosa cells secrete: estrogen progesterone inhibin
63
What is a red flag symptom and what are the causes for endometrial cancer?
RED FLAG - Postmenopausal bleeding ``` Obesity, Diabetes, Nulliparity, Late menopause, Ovarian Tumours (granulosa), HRT, Pelvic irradiation, Tamoxifen, PCOS, HNPCC ``` UNOPPOSED ESTROGEN
64
What are the investigations for suspected endometrial cancer?
History Examination Investigations: Transvaginal ultrasound Endometrial biopsy Hysteroscopy ``` Pathology: adenocarcinoma (most common), adenosquamous, squamous papillary serous clear cell uterine sarcomas ``` Staging: FIGO I/II/III/IV
65
What are the treatment options and 5 year survival for Endometrial cancer?
Surgery – hysterectomy +/- pelvic lymph nodes Radiotherapy – Adjuvant (brachytherapy/external beam). Progesterone therapy 5 year survival for Stage 1 disease = 80%
66
What is the Aetiology for cervical cancer?
High risk HPV ``` Early age intercourse (<16 years) Multiple sexual partners STDs Cigarette smoking – more persistent HPV Previous CIN Multiparity Oral Contraceptive Pill usage Other genital tract neoplasia ``` 75% population will be affected by HPV at sometime in their life Most infections are transient Age 20 - 25 20% HPV 16 positive Age 50 5% HPV 16 positive High risk HPV: >130 double-stranded DNA virus Oncogenic types – 16, 18, 31, 33, 45, 51, 53 ….. E6 and E7 oncoproteins are the main transforming gene products Persistent infection is associated with an increased risk of high grade cervical intraepithelial neoplasia (CIN 2, 3/HSIL) HIV and renal transplant patients at high risk due to reduced immune competence
67
What is the epidimeology for Cervical cancer?
Incidence – increasing women aged 25 – 29yrs in UK Most common cancer in women < 35 yrs in UK Majority diagnosed at stage 1 Pathology – squamous (90%) / adenocarcinoma Staging – FIGO I/II/III/IV Prognosis; stage I > 90% 5 year survival (1a1 = 98-99%, 1b2 = 82%)
68
What is the treatment for Cervical cancer?
stage 1: Local surgical excision of abnormal cells with Lletz loop Stage 2+: Radiotherapy Chemotherapy Palliative care
69
What is the aetiology and pathology of Vulval cancer?
``` Aetiology - VIN (HPV)/ Lichen Sclerosis Pathology - Squamous (90%) - Malignant melanoma - Bartholin’s gland, - Paget’s Disease Incidence - uncommon, 20th most common cancer in woman ```
70
How would Vulval cancer present?
``` Symptoms: Vulval itching Vulval soreness Persistent ‘lump’ Bleeding Pain on passing urine Past history of VIN or Lichen Sclerosis ```
71
What is the Vulval cancer staging and associated 5 year survival?
I <2cm (79% 5 yr survival) II >2cm (59% 5 yr survival) III Adjacent organs / Unilateral Nodes (43% 5 yr survival) IV Bilateral nodes / Distant mets (13% 5 yr survival)
72
What are the treatmetn options for Vulval cancer?
Surgery – Conservative Surgery – Radical Radiotherapy +/- chemo
73
How would Ovarian cancer present?
``` Bloating / ‘IBS’ like symptoms Abdominal pain/discomfort Change in bowel habit Urinary frequency Bowel obstruction No symptoms at all ```
74
What is the incidence and aetiology of Ovarian cancer?
Incidence > 7000 cases UK/year Aetiology Ovulation (menarche, menopause, parity, breast feeding, OCP, hysterectomy, ovulation induction) Gene mutation (BRCA 1/2, HNPCC) Over 50% present with advanced (stage 3 + disease), Stage 3 disease has 40% 5 year survival rate. ``` Pathology: Epithelial 85% Sex cord (e.g. Granulosa) Germ cell ( e.g. dysgerminoma, teratomas) Secondary (e.g. Krukenberg) ```
75
How would you investigate a suspected Ovarian cancer?
CA125 (Cancer Antigen 125 - blood test for ovarian cancer marker) Ultrasound (USS) Symptoms and age Referral based on Risk of Malignancy Index (RMI) = CA125 x USS score (1 or 3) x pre or post menopausal (1 or 3) RMI example: 70 year old woman with a solid cystic adnexal mass of 8cm with ascites and a CA125 of 400 RMI = 3 (postmenopausal) x 3 (more than one abnormal feature of cyst on USS) x 400 = 3600 A score of 250 + indicates referral to gynaecological oncologist
76
What is pre-eclampsia and eclampsia?
pre-eclampsia: New HT after 20th week (earlier with trophoblastic disease) - Systolic >140/ Diastolic>90 ``` Increased BP (gestational BP elevation) with proteinuria - ≥ 0.3g protein /24hr ≥ +2 on urine dip specimen ``` Oedema NOT part of definition Eclampsia: features of pre-eclampsia plus generalised tonic-clonic seizures It occurs when there is a failure of conversion of the spiral arteries into vascular sinuses resulting in placental ischaemia (this can cause fetal growth retardation). The placenta then produces thromboplastins (that can lead to DIC) and Renin which causes vasoconstriction and poor renal perfusion, leading to the symptoms of hypertension and protienuria (and oedema) that are characteristic of pre-eclampsia. if untreated there is increasing severity and subsequent eclampsia.
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Preeclampsia can be mild or severe. What are the clinical criteria for Severe Preeclampsia?
Clinical criteria for Severe Preeclampsia (one or more): ``` BP: >160 systolic, >110 diastolic Proteinuria: >5gm in 24 hrs, over 3+ urine dip Oliguria: < 400ml in 24 hrs CNS: Visual changes, headache, scotomata, mental status change Pulmonary Edema Epigastric or RUQ Pain Impaired Liver Function tests Thrombocytopenia: <100,000 Intrauterine Growth Restriction Oligohydramnios ```
78
What is HELLP syndrome and which disease state is it commonly associated with?
Haemolysis, Elevated Liver enzymes (ALT and AST), Low Platelet count It is a complication associated with preeclampsia
79
What are the symptoms of Preeclampsia?
``` Visual disturbances. Headache similar to migraine. Epigastric pain - hepatic swelling and inflammation, stretch of liver capsule ± Oedema Rapid weight gain ```
80
What are the physical finding upon examination in Preeclampsia?
High Blood Pressure Proteinuria Retinal vasospasm or oedema Right upper quadrant (RUQ) abdominal tenderness Brisk, or hyperactive, reflexes common during pregnancy Ankle clonus is a sign of neuromuscular irritability that raises concern.
81
State 2 differential diagnoses for preeclampsia
Thrombotic Thrombocytopenic Purpura Haemolytic Uremic Syndrome Acute Fatty Liver of Pregnancy
82
What laboratory test would you order if you suspected preeclampsia?
Haemoglobin, platelets (this would be reduced) Serum uric acid (this would be raised) Liver function tests If 1+ protein by clean catch dip stick Timed collection for protein and creatinine Accurate dating and assessment of fetal growth
83
The “cure” for preeclampsia is delivery however this may not always be favourable. What are the maternal and fetal indications for delivery?
``` Maternal: Gestational age 38 wks Platelet count < 100,000 cells/mm3 Progressive deterioration in liver and renal function Suspected abruptio placentae Persistent severe headaches, visual changes, nausea, epigastric pain, or vomiting . Fetal: Severe fetal growth restriction Nonreassuring fetal testing results Oligohydramnios ``` Delivery should be based on maternal and fetal conditions as well as gestational age Route of Delivery: Vaginal delivery preferable Labour induction (usually within 24 hours) Neuraxial (epidural, spinal, and combined spinal-epidural) techniques offer advantages Hydralazine or labetalol are pretreatments to reduce hypertension during delivery.
84
Apart from delivery, what other treatments are used in Preeclampsia?
Anticonvulsive Therapy: Indicated to prevent recurrent convulsions in women with eclampsia or to prevent convulsions in women with preeclampsia. Parenteral magnesium sulphate reduces frequency of eclampsia and maternal death (Caution in renal failure) If Systolic BP > 160 mm Hg and/or Diastolic BP > 105 mm Hg the following can be used: Parenteral hydralazine and labetalol (avoid in women with asthma and CHF) Oral nifedipine used with caution Sodium nitroprusside
85
What are the risk factors for Preeclampsia?
``` Young female X3 increased risk Blacks X2 increased risk Multifetal pregnancies Hypertension Renal Disease Collagen Vascular Disease ``` Risk of recurrent preeclampsia increases with: Preeclampsia before 30 weeks (40%) New father Blacks
86
What is the definition of a Premature infant?
Premature Infants born before: 37 weeks 259 days from LMP 245 days after conception ``` Prematurity is a major contributor to: developmental delay visual impairment chronic lung disease cerebral palsy ```
87
What is considered to be a Low Birth Weight (LBW) and what are the different categories of low birth weight?
``` LBW infants: <2500 g at birth regardless of gestational age Low Birth Weight: <2500gm Very Low Birth Weight: <1500gm Extremely Low Birth Weight: <1000gm ``` VLBW infants X10 more likely to be handicapped than >2500gm
88
What are the risk factors for pre-term birth?
``` Non-modifiable Race, Previous preterm birth multiple pregnancy previous cervical surgery IUGR preeclampsia medical comorbidities uterine anomalies ``` Modifiable: Genital infection - Bacterial vaginosis, 2-fold risk, studies conflicting Systemic Infection - UTI, Pyelonephretis, Appendicitis Cervical weakness Socioeconomics - Smoking
89
What are the Primary, Secondary and Tertiary Preventions for Pre-term birth?
``` Primary (Reducing population risk): Effective interventions not demonstrable yet Smoking and STD prevention Prevention of multiple pregnancy Planned pregnancy Variable work schedules Physical and sexual activity advice Cervical assessment at 20-26 weeks ``` Secondary (screening for pre-term labour) ; Transvaginal cervical ultrasound Qualitative fetal fibronectin test ``` Tertiary: Treatment after diagnosis Aim to reduce morbidity/mortality by: Prompt dx, referral Drugs - tocolysis, antibiotics Corticosteroids ```
90
What re the treatment options for the prevention of pre-term birth?
Consider tocolysis and give steroids Progesterone: Recent studies suggest benefit in women at high risk Given as IM injection or pessary Treatment principles: Identify associated cause, treat if possible Assess fetal maturity Decide the best route of delivery Plan with neonatalogists and in the best place. Consider in utero transfer
91
A 32 year old woman in her 1st pregnancy presents to your labour ward with a 4 hour history of intermittent lower abdominal pains and drainage of clear fluid par vaginam. You are the F1 Doctor around. How would you clerk and investigate?
Management of PROM (preterm rupture of membranes): Admit for 48hrs Rule out chorioamnionitis and sepsis - If evidence of chorioamnionitis, expedite delivery irrespective of gestational age Ix: temperature, MSU, high vaginal swab Give steroids for fetal lung maturity Give erythromycin 500mg PO QDS for 10 days to reduce neonatal morbidity 80% will go into labour in 24 hours. In 20% that do not go into labour spontaneously, discharge home after 48 hours (no tampons/sex/swimming) with weekly outpatient follow up with ESR and CRP. Aim for induction at 34 weeks. If infection develops then take blood cultures, Start Iv antibiotics (as for group b strep) and expedite delivery. ``` Biggest risks to the fetus are: INFECTION risks of prematurity (no surfactant ect...) pulmonary hypoplasia Limb contractures ``` ``` Risks of prematurity: Respiratory distress syndrome (RDS) Intraventricular hemorrhage (IVH) Patent ductus arteriosis (PDA) Necrotizing enterocolitis (NEC) Retinopathy of prematurity (ROP) Jaundice Anemia ```
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what are the complications associated with iron deficiency anaemia in pregnancy?
Iron deficiency is associated with low birthweight and preterm delivery Pregnancy is associated with a 2-3 fold increase in requirement for iron and a 10-20 fold increase in folate requirements Iron deficiency is the commonest anaemia followed by folate deficiency
93
What are the maternal and fetal risk of diabetes in pregnancy?
``` Maternal risks: Diabetic ketoacidosis Hypoglycaemia (common) Progression of retinopathy Pre-eclampsia Premature labour ``` Fetal/Neonatal risks: Miscarriage Macrosomia, shoulder dystocia Fetal abnormality Stillbirth (Cause of late stillbirth) Neonatal hypoglyaemia, respiratory distress, hypocalcaemia, polycycaemia Most fetal complications are thought to relate to maternal hyperglycaemia, excessive glucose transfer across the placenta and secondary fetal hyperinsulinaemia Key to optimising outcome is good glycaemic control from conception
94
What medications can be used to treat Diabetes in pregnancy?
Insulin – basal bolus regime Metformin (decreases hepatic gluconeogenesis and promotes increased insulin sensitivity) Glibenclamide (a sulphonylurea – increases pancreatic insulin secretion from beta cells) ( All other hypoglycaemics are contraindicated) Statins and ACE inhibitors are contraindicated.
95
What are the maternal and fetal risks of Renal disease in pregnancy?
``` Maternal risks: Severe hypertension Deterioration in renal function Pre-eclampsia Caesarean section ``` ``` Fetal/Neonatal risks: Premature delivery Growth restriction Stillbirth Abnormalities due to maternal drug therapy ```
96
What are the maternal and fetal risks of Epilepsy in pregnancy?
Maternal: Increase in seizure frequency – 25-33% Sudden Unexpected Death in Epilepsy (SUDEP) occurs in about 1 in 500-1000 people with epilepsy). SUDEP is more common in patients who do not take their prescribed anticonvulsants. Pregnant and breastfeeding women are often reluctant to take anticonvulsants for fear of harming their baby Fetal: Fetal/Neonatal abnormality - epilepsy is associated with a risk of fetal abnormality - mainly due to anticonvulsant medication, may also be due to epilepsy itself All anticonvulsants are associated with a risk of fetal abnormalities – Sodium Valporate has the highest risk - 7-9% Inheritance of epilepsy Risk of fetal hypoxia associated with maternal seizures Neural tube defects (offer pre-conceptual high dose folic acid)
97
What is the treatment of choice for Venous Thrombo-Embolism in pregnancy?
LMWH (warfarin crosses the placenta and may cause fetal abnormalities and intracranial bleeding)
98
What are the normal physiological respiratory, cardiac and renal changes in pregnancy?
Resp: Increased metabolic rate and 20% increase in O2 consumption Minute ventilation increases due to increase in tidal volume - respiratory rate unchanged Arterial pO2 increases and pCO2 decreases Mild compensated respiratory alkalosis is normal in pregnancy Cardiac: Cardiac output rises by 40% mainly due to increased stroke volume (CO=SV x HR) Renal: Pregnancy with healthy kidneys is associated with a 50% increase in renal blood flow and GFR. Serum creatinine, urate and albumin fall. The pelvicaliceal system and ureters dilate, predisposing to ascending infection and acute pyelonephritis
99
How does endometriosis present and what laboratory investigation would you perform?
Pain (Cyclic pain, Dysmenorrhoea, Dyspareunia) Infertility (due to Immune factors, Oocyte toxicity, Tubal dysfunction, Ovarian dysfunction, Adhesions) CA125 - would be raised Generally a young, nulliparous patient
100
What are the treatment options for endometriosis?
Medical: OCP GnRH agonists Oral progestagens Depot Provera Mirena ``` Surgical: Ablation Excision Oophorectomy Pelvic clearance ```
101
What is adenomyosis?
Adenomyosis is a condition in which the inner lining of the uterus (the endometrium) breaks through the muscle wall of the uterus (the myometrium) The symtoms are very similar to endometriosis: Pain (Cyclic pain, Dysmenorrhoea, Dyspareunia) but the patients tend to be Older and Multiparous
102
What are uterine fibroids?
``` Benign uterine tumours Smooth muscle tumours Variable size and number Prevalence: 30% of women above 30 Oestrogen dependant ``` ``` They can be: Pedunculated Intramural Subserosal Submucosal Intracavitary ``` Treated be either laparoscopic or hysteroscopic myomectomy
103
What are the symptoms of Uterine Fibroids?
``` Asymptomatic Heavy periods Anaemia Infertility Miscarriage ```
104
How do you record a womans Gravidity and Parity?
TOTAL no. of pregnancies (including this one, multiple pregnancies count as one) = Gravidity (G) TOTAL no. of deliveries after 24 weeks = Parity (P) Expressed as G_P_ + indicates a pregnancy loss before 24 weeks – indicates a loss after 24 weeks (including neonatal)
105
What is a miscarriage?
Miscarriage = loss of pregnancy before 24 weeks
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What is an IUFD?
Intra Uterine Fetal Death: Babies with no sign of life in utero
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What is a stillbirth?
Stillbirth: Baby delivered with no signs of life, known to have died after 24 completed weeks of pregnancy
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What is a neonatal death?
Neonatal death: The death of a baby within the first 28 days of life Early NND: Up to 7 days Late NND: Between 7 and 28 days
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Define Term, Pre-term and Post-term
``` Term = 37 to 42 completed weeks gestation Pre-term = < 37 weeks gestation Post-term = > 42 weeks gestation ```
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Define Macrosomia
>4.0kg Large for dates (LFD) or macrosomia
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What are the causes of Antepartum Haemorrhage?
Low lying placenta/placenta praevia - Classically painless and can be large amount. - Maternal compromise may be swift Placenta accreta Vasa praevia (fetal blood vessels cross or run near the internal opening of the uterus) Minor/major abruption (a serious condition in which the placenta partially or completely separates from the uterus before delivery) - Classically painful but bleeding out of keeping with maternal shock Infection Unexplained
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What is placenta praevia?
Any part of the placenta that has implanted into the lower segment of the uterus Minor – in lower segment/encroaching upon the cervical os Major – covering/reaching cervical os Minor praevia repeat scan at 36 weeks (TV) Major praevia repeat scan at 32 weeks (TV) Placenta must be >25mms from cervical os < 25 mms from cervical os repeat scan Placenta remains < 25 mms elective caesarean section
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What is the management for placenta praevia?
Advise the symptoms to watch for Seek advice early Outpatient management if asymptomatic If recurrent bleeds, may need admission until delivery with weekly X match Increased risk of iatrogenic preterm delivery if large bleed Remember Anti D if Rhesus negative Elective caesarean section at 38 -39 weeks ``` Minor Bleed: 15 minute observations – BP, pulse, temp, O2 saturations, urine output (catheterise) Examination - General and abdominal - Vaginal (avoid digital examination) ? USS (check 20 week scan) Fetal monitoring (CTG) +/- arrange delivery Steroids if < 34 weeks gestation ``` ``` Major Bleed: Resuscitate by ABC Two 14/16 G cannulas – antecubital fossa Crystalloid X-match 6 units FBC, U&E, LFTs, Clotting Consultant Obstetrician and Anaesthetist (Neonatologist) ```
114
What is the most appropriate management for suspected placenta accreta?
20 week scan watch for anterior Placenta praevia and placenta accreta - Loss of definition between wall of uterus and Abnormal vasculature Perform MRI scan Elective caesarean section 36 to 37 weeks Risks: haemorrhage, transfusion, caesarean hysterectomy, ITU admission
115
What is Vasa praevia?
Fetal vessels coursing through the membranes over the internal cervical os and below the fetal presenting part, unprotected by placental tissue or the umbilical cord 1 in 2,000 to 6,000 pregnancies No major maternal risk, but major fetal risk Membrane rupture leads to major fetal haemorrhage CTG abnormalities Mortality 60%
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What is placental abruption?
Premature separation of the placenta from the uterine wall Concealed or revealed haemorrhage Woody-hard, tense uterus Fetal distress Maternal shock out of proportion to bleeding Small abruptions may be managed conservatively Large abruptions need resuscitation and delivery
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What are the risk factors for placental abruption?
``` Previous abruption Hypertension Multiple pregnancy Trauma - Medical e.g. amniodrainage, ECV - Trauma e.g. RTA, domestic violence Vasoconstrictor drugs e.g. cocaine and crack Infection Thrombophilias Uterine abnormality Smoking ```
118
Define Post-Partum Haemorrhage and state 5 risk factors
Primary: - Within 24 hours of delivery, blood loss > 500mls Secondary: After 24 hours and up to 12 weeks post delivery Minor (500 -1000 mls) Major (> 1000 mls) Major cause of maternal death worldwide. Total blood volume at term is approximately 100mls/kg. For a woman of 70kg a blood loss of more than 40% of her total blood volume (2,800mls) is generally regarded as life threatening. ``` Risk Factors: Big baby Nulliparity and grand multiparity Multiple pregnancy Precipitate or prolonged labour Maternal pyrexia Operative delivery Shoulder dystocia Previous PPH ```
119
What are the causes of Post-Partum Haemorrhage?
``` The four ‘T’s - Tissue – ensure placenta complete - Tone – ensure uterus contracted, syntometrine, syntocinon, ergometrine, haemobate, misoprostol - Trauma – look for tears and repair - Thrombin – check clotting ```
120
State 5 risk factors for Venous Thrombo-Embolism in pregnancy and describe how the risk is managed
``` Previous VTE Inherited and acquired thrombophilia Medical comorbidities Age > 35 BMI > 30 Smoking Parity > 4 Multiple pregnancy Pre eclampsia Caesarean section Hyperemesis Immobility Systemic infection ``` VTE is currently leading direct cause of maternal mortality Usually preventable with appropriate thromboprophylaxis (LMW heparin and TEDS) Highest risk in the postpartum period Prophylactic dose of LMW heparin given according to maternal weight
121
State 5 risk factors for maternal sepsis
Obesity Diabetes Impaired immunity/ immunosuppressant medication Anaemia Vaginal discharge History of pelvic infection History of group B streptococcal infection Amniocentesis and other invasive procedures Cervical cerclage Prolonged spontaneous rupture of membranes GAS infection in close contacts / family members
122
What is the management for Eclampsia?
The onset of seizures in a woman with pre-eclampsia Any seizures in a pregnant woman are eclampsia until proven otherwise IV MgSo4 4gms given over 5 minutes, followed by an infusion of 1 g/hour maintained for 24 hours Recurrent seizures - further dose of 2–4 g given over 5 minutes Treat hypertension – labetalol , nifedipine , methyldopa, hydralazine Stabilise mum, deliver baby
123
What are the risk factors for cord prolapse and why is it an emergency?
``` Premature rupture membranes Polyhydramnios (having a large volume of amniotic fluid) Long umbilical cord Fetal malpresentation Multiparity Multiple pregnancy ``` Cord prolapse occurs when cord is presenting and there is membrane rupture. Exposure of the cord leads to vasospasm which can cause significant risk of fetal morbidity and mortality from hypoxia.
124
What is the management for cord prolapse?
Call 999 (if not in hospital) Infuse fluid into bladder via catheter if at home Trendelenburg with knees and hips up Constant fetal monitoring Alleviate pressure on cord - push PP off cord Transfer to theatre and prepare for delivery
125
What is shoulder dystocia?
Failure for the anterior shoulder to pass under the symphysis pubis after delivery of the fetal head that requires specific manoeuvres to facilitate delivery Approx 1% of pregnancies Intrapartum emergency High risk for maternal and fetal morbidity Can cause fetal mortality
126
What are the risk factors for shoulder dystocia?
``` Macrosomia (most SD occur in normally grown babies) Maternal diabetes Disproportion between mother and fetus Postmaturity and induction of labour Maternal obesity Prolonged 1st or 2nd stage of labour Instrumental delivery ```
127
What is the management for shoulder dystocia?
``` H – Call for help (emergency buzzer) E – Evaluate for episiotomy L – Legs in McRoberts P – Suprapubic pressure E – Enter pelvis R – Rotational manoeuvres R – Remove posterior arm (R – Replace head and deliver by Lower segment Cesarian section (LSCS) -Zavanelli) ```
128
What are the maternal and neonatal complications of shoulder dystocia?
Maternal - PPH - Extensive vaginal tear (3rd and 4th degree) - Psychological Neonatal - Hypoxia - Fits - Cerebral palsy - Injury to brachial plexus (erbs palsy)
129
Define Menarche
Menarche age 12-13 (11-14.5 in 95%) Preceded by development secondary sexual characteristics, and peak height velocity Initial cycles usually anovulatory - pain free and often long gaps between Bleeds last 3-7 days 21-45 day gaps
130
Define primary and secondary amenorrhoea
Primary: no menses by age 16 in the presence of secondary sexual characters (Hypothalamic; pituitary; ovarian- Turners, POF, Swyer sydrome; anatomical; enzyme/receptor-CAH, CAI) In the absence of secondary sexual characters: 13 years Secondary: cessation after onset of menses (wt loss, excessive exercise, PCOS) Oligomenorrhoea: menses more than 35 days apart
131
Define precocious puberty
appearance of physical and hormonal signs of pubertal development at an earlier age than is considered normal Puberty before age 8 (girls) 9 (boys) secretion of high-amplitude pulses of gonadotropin-releasing hormone (GnRH) by the hypothalamus
132
What are the different types of precious puberty?
Central: gonadotropin-dependent: maturation of the entire HPG axis (spectrum of physical and hormonal changes of puberty) CNS abnormalities: trauma, tumors, hydrocephalus Pseudopuberty: gonadotropin-independent CAH, tumors of the adrenals, ovaries, Mc-Cune Albright syndrome
133
What is Mc-Cune Albright syndrome?
A disorder that affects the bones, skin, and several endocrine tissues. People with McCune-Albright syndrome develop areas of abnormal scar-like (fibrous) tissue in their bones, a condition called polyostotic fibrous dysplasia. McCune–Albright syndrome is suspected when two or more of the following features are present: Fibrous dysplasia Café au lait macules, including characteristic jagged "coast of Maine" borders and tendency not to cross the midline Hyperfunctioning endocrine disease The clinical presentation of patients with McCune Albright Syndrome varies greatly depending on the disease features. Associated endocrine abnormalities Precocious puberty: The most common endocrinopathy is precocious puberty, which presents in girls (~85%) with recurrent estrogen-producing cysts leading to episodic breast development, growth acceleration, and vaginal bleeding. Precocious puberty may also occur in boys with McCune–Albright syndrome, but is much less common (~10-15%). Testicular abnormalities: Testicular abnormalities are seen in a majority (~85%) of boys with McCune-Albright Syndrome. Hyperthyroidism: Hyperthyroidism occurs in approximately one-third of patients . Many others may suffer from other kinds of thyroid involvement. Growth Hormone Excess: GNAS mutation in the anterior pituitary can result in excess growth hormone secretion and is found in approximately 10-15% of patients. Cushing's Syndrome is a very rare feature that develops only in infancy.
134
Define peurperium
The time from the delivery of the placenta to six weeks following the birth
135
What is Lochia?
the vaginal discharge after giving birth containing blood, mucus, and uterine tissue. Lochia discharge typically continues for 4 to 6 weeks after childbirth, which is known as the postpartum period. ``` Lochia Rubra - day 0-4: Blood Cervical discharge Decidua Fetal membrane Vernix Meconium ``` ``` Lochia Serosa - day 4-10: Cervical mucus Exudate Fetal membrane Micro-organisms White blood cells ``` ``` Lochia Alba - day 10-28: Cholesterol Epithelial cells Fat Micro-organisms Mucus Leukocytes ```
136
Describe the normal physiological changes following delivery
Imediately after birth, the uterus contracts down fully and the fundus is felt at the level of the umbilicus. On average the fundus height decreases by about 1cm per day, and has returned to the true pelvis by day 10. The muscle layer returns to normal thickness by process of ischaemia, autolysis (removal of redundant actin and myosin fibres by proteolytic enzymes and macrophages) and phagocytosis (removal of excess fibrous and elastic tissue). The decidua is shed as lochia, and the endometrium regenerates. The biggest change in size of uterus happens in first 10 days , but not complete until about 6 weeks. The vagina, uterine ligaments and muscles of the pelvic floor also return to pre-pregnant state. Cervix – internal os closed by 2nd week, external os dilate a finger for weeks/months or permanently.
137
What is colostrum?
Colostrum – is very rich in proteins, vitamin A, and sodium chloride, but contains lower amounts of carbohydrates, lipids, and potassium than mature milk. The most important bioactive components in colostrum are growth factors and antimicrobial factors. The antibodies in colostrum provide passive immunity, while growth factors stimulate the development of the infant gut. They are passed to the neonate and provide the first protection against pathogens Lactogenesis 2 starts from expulsion of placenta and withdrawal of pregnancy hormones (particularly progesterone). Normally by 72hrs (48-72)
138
Which hormones are involved in the process of lactation?
Prolactin – milk production Oxytocin – Milk ejection reflex Insulin and cortisol Baby suckles -> Sensory impulses pass from the nipple to the brain -> Prolactin secreted by anterior pituitary gland and Oxytocin secreted by posterior pituitary gland. These hormones travel via bloodstream to the breasts -> Prolactin: Lactocytes produce milk Oxytocin: Myo-epithelial (muscle) cells contract and expel milk
139
What is the role of lactoferrin in breast milk?
Schematic figure of the iron-binding site of lactoferrin. The iron atom is shown as a red sphere, while the interacting amino acid residues of lactoferrin are in yellow. Lactoferrin is an iron-binding diferric glycoprotein present in most of the exocrine secretions. The major role of lactoferrin, which is found abundantly in colostrum, is antimicrobial action for the defense of mammary gland and the neonates. Lactoferrin consists of two equal halves, designated as N-lobe and C-lobe, each of which contains one iron-binding site. Human milk is unusually rich in lactoferrin, the normal concentration ranging from abo4t 7 mg/ml in colostrum to not less than 1 mg/ml in mature milk. The ability of lactoferrin to inhibit the growth of certain micro-organisms in vitro has been well documented. Most interest has focused on enteropathogenic strains of Escherichia coli, Staphylococcus albus, Staphylococcus aureus, Pseudomonas and Candida albicans.
140
What are the parameters that indicate sepsis in pregnancy or post partum?
"3 Ts white with sugar" 2 or more of the following: ``` Temperature <36 or >38 degrees Tachycardia -Heart rate > 90bpm (PN) Tachypnoea - Respiratory rate > 20bpm WCC >12 or <4 x 109/l Hyperglycaemia >7.7mmol ``` ``` Other signs: PROM/offensive liquor Offensive lochia Catheter or dysuria Headache + neck stiffness Cellulitis/wound infection D and V Breast redness or pain Cough, sputum, chest pain Abdominal pain ```
141
What is the management for sepsis in pregnancy or post partum?
Sepsis 6 (BUFALO) plus 2: Bloods cultures - plus fbc, u+e, lfts, clotting, glucose, crp, blood gases(and consider other swabs) Urine output <30ml hour - monitor Fluid Resuscitation - bolus of hartmans or saline to max 60ml/kg Antibiotics - Broad spec IV within the hour (ASAP!) Lactate - if >2 mmol/l with sign of organ failure contact ITU Oxygen <90% - give high flow Plus 2 – Consider delivery (Evacuation of Retained Products of Conception) & VTE prophylaxis
142
what are the risk factors for post partum urinary retention?
``` Epidural analgesia Prolonged second stage of labour Forceps or ventouse delivery Extensive perineal lacerations Poor labour bladder care ```
143
What are the leading causes for direct and indirect maternal death?
75% of maternal deaths are postnatal Overall there was no statistically significant decrease in the maternal death rate in the UK between 2010–12 and 2013–15. Maternal deaths from direct causes remain unchanged The rate of indirect deaths is reduced Thrombosis and thromboembolism remains the leading cause of direct maternal death Cardiac disease the leading cause of indirect maternal death Maternal suicides were reclassified by the World Health Organisation as a direct cause of maternal death.