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Med 3 > Pregnancy Complications, Fetal Morbidity And Assisted Reproduction > Flashcards

Pregnancy Complications, Fetal Morbidity And Assisted Reproduction Flashcards

1
Q

Hypertension during pregnancy

A

5-10% of pregnancies
BP > 140/90 on 2 occasions 6 hours apart
Hypertension needs to be controlled to prevent organ damage in long term

Hypertension present at booking is not pre eclampsia

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2
Q

What is chronic hypertension

A

Present at booking or before 20 weeks

No significant proteinuria

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3
Q

What is gestational hypertension

A

Presenting after 20 weeks with no significant proteinuria

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4
Q

What is pre eclampsia

A

Hypertension present at 20 weeks and significant proteinuria

Caused by pregnancy
Cured by delivery of placenta
Endothelial cell disorder
Excessive inflammatory response to pregnancy

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5
Q

Features of pre eclampsia

A 
Hypertension 
Proteinuria 
Oedema 
Multi organ involvement 
Fetal compromise
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6
Q

Risk factors socio demographic for pre eclampsia

A

Extremes of reproductive age

Ethnic groups

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7
Q

Risk factors for pre eclampsia (pregnancy factors)

A

Multiple pregnancy
Primigravida
Assisted conception
Previous pre eclampsia

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8
Q

Abnormal placentation

A

Trophoblast cells fail to invade into maternal endometrium and myometrium

Maternal spinal arteries: persistent thick muscular walls
Reduced perfusion of placenta with maternal blood and possible vasospasm
Leads to increased apoptosis (cell death)
Release of circulating factors or placental syncytial fragments

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9
Q

Endothelial cell dysfunction

A

Increased capillary permeability - tissue oedema

Hypertension secondary to disturbed control of vascular tone by endothelial cells
Altered production of vasodilator substances

Clotting dysfunction secondary to abnormal production of procoagulants by endothelial cells, activation and clumping of platelets

Plasma volume loss and organ hypoperfusion

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10
Q

Symptoms of pre eclampsia

A

Headache: usually frontal but may be occipital due to cerebral oedema and hypertension

Visual disturbances: blurred, flashes of light or blindness

Epigastric or right upper quadrant pain due to enlargement of subcapsular haemorrhage of liver

Nausea and vomiting due to congestion of gastric mucosa and or cerebral oedema

Oliguria or anuria due to kidney pathology

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11
Q

Maternal complications of pre eclampsia

A

Neurological: seizures, retinal detachments, cortical blindness, intra cerebral or subarachnoid haemorrhage

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12
Q

Cardiovascular complications of pre eclampsia

A

LVF, pulmonary oedema, hypertension

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13
Q

Fetal complications of pre eclampsia

A 
Asymmetrical FGR 
Intrauterine hypoxia 
Prematurity 
Abruption 
Still birth 
Hypertension / metabolic disease in later life
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14
Q

Maternal monitoring for pre eclampsia

A 
BP 4-6 hourly 
Urinalysis 
Symptoms and signs 
Blood tests (FBC, U&E, LFT, fibrinogen) 
Fluid balance
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15
Q

Fetal monitoring for pre eclampsia

A 
Movements 
U/S Size and growth 
Umbilical artery Doppler 
Liquor volumes 
Biophysical tests 
CTG >26 weeks monitoring of fetal heart beat
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16
Q

Drug targets for pre eclampsia

A

Aim to keep BP <150/100mmHG
Decreases the maternal cerebral and cardiovascular complications but not fetal outcomes
Consider MgSO4 to reduce risk of seizures and mortality
Death rate is now less than 1:1,000,000

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17
Q

How often should you test sugars in diabetes in pregnancy

A

Depends on severity but usually before and after a meal and before bedtime (7 times)

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18
Q

Changes in carbohydrate metabolism in normal pregnancy

A

Feto placental unit uses glucose therefore lower fasting blood glucose

Peripheral resistance to effects of insulin due to hormones eg HPL from the placenta, oestrogen, progesterone, cortisol

Insulin resistance increases with gestation

Mostly higher post prandial glucose

Diabetes occurs if B cells of pancreas are unable to produce sufficient insulin to prevent hyperglycaemia

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19
Q

Prevalence of diabetes in pregnancy

A

5-10% of all pregnancies in UK

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20
Q

Screening for gestational diabetes

A

Incidence increasing

Selective screening misses up to 30% of cases

Test: 2 hour 75g oral glucose tolerance test 24-28 weeks

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21
Q

Risk factors for GDM

A

BMI above 30

Previous macrosmic baby weighing mroe than 4.5kg

Previous gestational diabetes

First degree relative with diabetes

Family origin with high prevalence eg south Asian, black Caribbean or Middle Eastern

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22
Q

Effect of pregnancy on diabetes

A

Greater importance of tight glucose control (target HbA1c <6,5%)
Change in eating pattern
Hypoglycaemia more common
May lose warning signs for hypos (vomiting)
Increase in insulin dose requirements at 18-28 weeks
Increased risk of severe hypoglycaemia
Risk of deterioration in pre existing retinopathy
Risk of deterioration of established nephropathy
Lower renal threshold for glycosuria

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23
Q

How to achieve good glycaemic control

A

Regular meals and snacks including late night supper (high fibre improves maternal sensitivity to insulin)

Regular capillary blood glucose tests

Medication, often multiple injections of insulin

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24
Q

Effects of diabetes on pregnancy

A 
Hypoglycaemia 
UTI 
Recurrent vulvovaginal candidiasis 
Pregnancy induced hypertension / pre eclampsia
Pre term labour 
Obstructed labour 
Operative deliveries 
Increased retinopathy 
Increased nephropathy 
Cardiac disease
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25
Q

Fetal growth in diabetes disorders

A

Macrosomia is >90th centile birth of more than 4000g

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26
Q

What is asignificant proteinuria

A

> 300mg protein in a 24 hour urine collection or >30mg/ml in a spot urinary protein: creatinine sample

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27
Q

Personal medical history risk factors for pre eclampsia

A 
Obesity 
Chronic renal disease 
Chronic hypertension 
DM and connective tissue diseases 
Certain thrombophilia
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28
Q

Respiratory maternal complications of pre eclampsia

A

Laryngeal oedema, respiratory distress syndrome (ARDS)

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29
Q

Hepatic maternal complications of pre eclampsia

A

Hepatocellular dysfunction, ischaemia pain, subcapsular haemorrhage and liver rupture

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30
Q

Renal maternal complications of pre eclampsia

A

Oliguria, renal failure (cortical or tubular necrosis)

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31
Q

Haematological maternal complications of pre eclampsia

A

Thrombocytopaenia, haemolytic, HELLP, DIC, thromboembolism

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32
Q

Drugs used fore emergency blood pressure control

A

Hydralazine, labetalol, nifedipine SR

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33
Q

Lifestyle changes as a first line Rx in GDM

A

Diet:
1 hour post prandial glucose strongly associated with birth weight: target level 7.8mmol/L
Inverse relationship between birth weight and proportion of dietary energy obtained from carbohydrate

Exercise: beneficial effects on glucose metabolism and reduces weight gain

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34
Q

Fetal growth in diabetes

A

High maternal blood glucose crosses placenta and stimulates fetal insulin production which acts as a growth promoter (bone, muscle, adipose tissue)

Excess glucose is laid down as glycogen in liver and adipose tissue

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35
Q

Different parts of the ovary

A

Outer covering of epithelium continuous with pelvic peritoneum

Stroma: support and hormones

Gamete producing structures

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36
Q

Different parts of the cervix

A

Endocervix: mucus secreting columnar epithelium

Ectocervix: stratified squamous epithelium

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37
Q

Different parts of uterus

A

1) endometrium - cuboidal epithelium overlying stroma

2) myometrium : smooth muscle

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38
Q

Most common type of tumour in the uterus

A

Affects the endometrium (glands) most often an adenocarcinoma

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39
Q

Normal cellular changes in the cervix

A

Occur at puberty, pregnancy and cyclical changes

Repositioning of the squamo-columnar junction exposes columnar cells to low pH environment of the vagina

Red appearance of exposed columnar cells - ectopy

Squamous metaplasia of cells in this transformation zone

These cells are vulnerable to dysplasia and neoplasia

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40
Q

Abnormal cellular changes in the cervix

A

Detected by Pap smear
‘Smear’ of desquamated cells on a slide from a spatula (being replaced by liquid cytology)

CN I - mild dysplasia (lower 1/3 epithelial thickness)
CIN II- moderate dysplasia (lower 2/3 epithelial thickness)
CIN III- severe dysplasia and carcinoma in situ (upper 1/3 and full thickness but intact BM)

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41
Q

Appearance of CIN cells

A

Increased nuclear to cytoplasmic ratio, clumped chromatin and a clear zone around the nucleus indicative of HPV infection

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42
Q

What does CIN stand for

A

Cervical intraepithelail neoplasia

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43
Q

Cervical cancer risk factors

A 
Sexual intercourse (HPV infection) 
Age of first intercourse 
History of STD 
Socioecomic status 
Smoking
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44
Q

What are uterine neoplasms

A

Benign

  • polyps (epithelial)
  • fibroids (smooth muscle - leiomyoma)
Malignant 
- uterine carcinoma 
- risk factors: 
Obesity 
Diabetes 
Hypertension 
Infertility
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45
Q

What is endometriosis

A

Ectopic and endometrial material that is under the influence of cyclic hormones

Occurs anywhere but commonly in Fallopian tubes and Adnexa

Theories include retrograde menstruation / differentiation of stem cells
Up to 10% of women
Can be very disabling and painful even when just a few foci are present
Leads to chronic cyclical inflammation, scarring and adhesions
May impact fertility

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46
Q

Describe ovarian tumours

A

5th most common cancer in women
5th cause of cancer death in women
Complex pathology due to abundance of pluripotent and totipotent cell types

Risk factors:
Nuliparity
Family history BRAC1 and 2 gene mutations

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47
Q

Where are ovarian tumours derived from

A

Surface epithelium 70%
Stroma 10%
Follicles (germ cells) 20%
Metastases from elsewhere

Presenting symptoms: none until advanced
Staging, treatment and prognosis as we go along

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48
Q

Staging of ovarian cancer

A

Stage 1: limited to ovary
Stage 2: involvement of other pelvic structures
Stage 3: intra abdominal spread beyond pelvis
Stage 4: distant metastases

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49
Q

What are teratomas

A

Neoplasms of germ cell origin
90% are benign and occur in patients <20
Mixture of mature tissues mainly derived from ectoderm- hair, skin, skin appendages and teeth

Can occasionally have tissues derived from endoderm and mesoderm
Presence of immature (less differentiated) tissues indicates malignancy - rare

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50
Q

Functions of breast

A

Provision of food

Provision of nursing, extended period of parental care and proximity

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51
Q

Risk factors for breast cancer

A

Cyclical changes in oestrogen and progesterone

Ageing

Can be hereditary (mutation in BRCA1 and BRCA2 genes- more frequent screening - mammography and MRI)

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52
Q

Describe area of breast

A

Highly modified area of skin with specialised sweat glands which produce nutritious secretions under hormonal influences

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53
Q

Ductal system within a mammary lobule

A

Each ductal system in a lobule ends in a cluster of blind ending terminal ductules. These blind ends will transform to alveoli at pregnancy and produce milk at lactation

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54
Q

Nipple, lactiferous duct and extra lobular ductal system

A

Extra lobular ducts from mammary lobules drain into lactiferous ducts

Lactiferous sinus (dilated milk can gather here during lactation)

Lactiferous duct opening into nipple (arranged in a ring, normally plugged with keratin)

Nipple (pigmented, raised skin which darkens after pregnancy)

Areola (melanin pigmentation, sebaceous gland and pressure receptors)

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55
Q

Development of the breast

A

1) fetus / neonate, male / female before puberty. Minimal ductal system
2) puberty- branching of ductal system, blind ends of ducts form small solid spheroidal masses of cells. Increase in fibrocollagenous and adipose tissue with successive exposure to oestrogen
3) pregnancy - formation of alveoli in terminal ductules. Hypertrophy of ductal lobular alveolar system.

4) lactating breast: secretion of milk from alveoli. Pituitary prolactin and oxytocin
5) resting - regressing of alveoli and ductal system

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56
Q

Breast changes in pregnancy

A

Under the influence of the placental hormones: progesterone, oestrogen, prolactin

Increase in vascularity and melanin pigmentation in the nipple and areola
Hyperplastic proliferation of terminal ductile epithelium, vacuoles in luminal epithelial cells, formation of true alveoli

2nd and 3rd trimester of pregnancy: increasing lipid rich proteinaceous secretion into alveoli
Increase in support tissue

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57
Q

Lactating breast (after parturition)

A

After parturition, progesterone levels drop, prolactin receptors are now expressed on surface of breast alveolar cells
True milk production can begin

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58
Q

What is milk fat

A

Synthesised in the smooth ER of the alveolar epithelial cells
Membrane bound droplets traffic towards the lumen

Droplets pinched off and released

Milk protein passes through golgi system into vacuoles and is released by exocytosis to the lumen

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59
Q

Female breast in resting (non secreting state)

A

Alveoli can still be distinguished

Evidence of mechanical atrophy

Alveolar distension, capillary occlusion and alveolar hypoxia leads to gradual involution. The ductule system rather than alveolar system again predominates

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60
Q

Preparations for postnatal nutrition

A

1) inhibition of expression of prolactin receptors by pregnancy levels of oestrogen and progesterone. This makes placental prolactin ineffective as far as lactogenesis is concerned
2) the drop in levels of oestrogen and progesterone after expulsion of placenta allows dominance of mothers pituitary prolactin and this activates alveolar prolactin receptors

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61
Q

Suckling induced reflex

A

When baby suckles, sensory information causes release of the neuropeptide prolactin from anterior lobe of pituitary gland. This then causes more milk production

Nipple stimulation by sucking is essential for keeping prolactin levels high

Strength and duration of suckling influences amount of prolactin released
Cessation of breast feeding results in inhibition of lactation

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62
Q

Psychosocial advantages of breast milk

A

Breastfeeding enhances attachment; frequent direct skin, smell, visual contact between newborn and mother

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63
Q

Disadvantages of breast feeding

A

Most drugs and alcohol taken by mother are transmitted through breast milk
Mums poor nutritional, physical or mental health or personal aversion to breast feeding may be a contraindication to nursing

Transmission of HIV can be halved by bottle feeding
(WHO recommends breast feeding up to 12 months with anti viral treatment)

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64
Q

What is gestational preparatory behaviour

A

Nest building

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65
Q

What is post parturient behaviour

A

Providing warmth, comfort, food and protection
Baby: need for contact, clinging, olfactory and rooting response in babies, characteristic cry patterns
Retrieval from harm, carrying baby with you etc

66
Q

What is weaning behaviour

A

Leads to gradual gain of independence

Mother / fathers proximity allows infants to resolve explore-retreat tendencies

67
Q

Why are infections different in pregnancy

A

Physiological / immunological changes may increase susceptibility eg stasis in urinary tract and alter clinical manifestations

Many drugs are contraindicated in pregnancy

68
Q

Consequences of infections in pregnancy

A

Infection of the fetus may have catastrophic consequences on fetal development
Neonatal immune systems not fully mature at birth, therefore infection may be devastating
Congenital infection may give rise to long term life threatening consequences eg blood borne viruses

69
Q

UTI in pregnant women

A

May be asymptomatic
May lead to pyelonephritis

Women are screened during pregnancy so can be detected early

70
Q

Varicella (chickenpox) in pregnant woman

A

More dangerous
Can cause varicella pneumonia ( more likely in pregnancy)
Antivirals are not licensed for use in pregnancy

71
Q

Cytomegalovirus (CMV) in pregnancy

A

Common infection
Almost always asymptomatic but can be life threatening in pregnancy - can cross placenta and infect fetus
Baby born with rash and hepatomegaly and enlarged spleen

3-4 per 1000 live births
5-10% half evident at birth
5% minor eg unilateral deafness

72
Q

Why is screening of CMV not advocated

A

1) there is no sensible advice to give to seronegative women
2) recurrent CMV infection may also cause symptomatic congenital infection

73
Q

Maternal rash in pregnancy

A

Must exclude maternal rubella - risk of congenital rubella syndrome - cataracts, heart problems
First 12 weeks - baby severely affected
12-18 weeks - most likely deafness
After 18 weeks - no risk

74
Q

Parvovirus B19

A

Most likely diagnosis with a maternal rash in pregnancy

  • no congenital parvovirus syndrome
    Increased risk of miscarriage (if not baby will be fine)
    Can cause fetal hydrops ( affects cells that cause red blood cells - baby becomes anemic - heart failure - fluid retention)
75
Q

Congenital toxoplasmosis

A

Transplacental transmission during maternal infection - risk increases with duration of pregnancy

Leads to brain damage, choroido-retinitis (may not present until later in life) carried in cat faeces, pregnant women advised not to change cat litter
Risk of fetal damage greatest in early pregnancy

76
Q

Congenital syphilis

A

May be multi system
Range of clinical features which present at 5-15 years
Hence routine antenatal screening and treatment

77
Q

Congenital varicella aka varicella embryopathy

A

Skin loss, scarring, usually unilateral, segmented
Impaired limb bud development
Many others, less specific features eg microcephaly, cataracts

78
Q

Zika virus infection

A

Outbreak in Brazil with coincident rise in reports of microcephaly
Evidence linking zika to fetal damage is convincing
Magnitude of risk unknown likely to be in the order of 1-10% if maternal infection in first trimester- impairment of brain development

79
Q

Blood borne virus infections

A

HIV
Hep B, C
Transmission may arise antenatally, perinatally (birth canal), postnatally

80
Q

Mother to baby HIV

A

Overall risk around 20%
Almost entirely preventable by maternal antiretroviral therapy to reduce viral load
Elective c section
No breast feeding

81
Q

Mother to baby hep B

A

Neonatal infection leads to very high carriage rates

Preventable by vaccine

82
Q

Mother to baby hep C

A

Rates very low compared to hep B eg 3-5%
No intervention
Therefore no rationale for screening

83
Q

Neonatal septicaemia / meningitis

A

Baby coming out of birth canal may be contaminated with organisms from maternal gut
Group B streptococcus, E. coli
Known carried of group B strep are given antibiotics during labour

84
Q

Group B strep

A

Important cause of neonatal pneumonia septicaemia and meningitis
Commonly found as normal GI flora
Colonises perineum / vagina in around 1/4 pregnant women

If colonised risk of c. 1/200 of neonatal infection
IV antibiotics during delivery reduces risk to 1/4000

85
Q

Management of maternal chickenpox in late pregnancy

A

Delivery > 7 days after onset maternal rash - nothing
VZIg to neonates born within 7 days of onset of maternal rash
Prophylactic acyclovir

86
Q

Neonatal herpes

A

Most infections acquired from primary maternal genital herpes at term
50% cases have internally disseminated infection without external lesions

Transmitted by someone with a cold sore kissing a baby

87
Q

Opthalmia neonatorum

A

Infection of conjunctivae with discharge
Caused by gonorrhoea or staphylococcus - acquired from mother
Can cause neonatal pneumonia

88
Q

What does it mean if there is a break or a crack in Shentons line

A

A sign of a femoral neck fracture

89
Q

Air in X-rays

A

Should only be seen in stomach, bowel and lung bases
Air outside of these regions is invariably pathological
Appearance of free air can differ according to the position of the patient

90
Q

Why is good communication with children important

A

Makes treatment easier
Child more cooperative, less upset, mroe likely to follow instructions
Helps doctor reach a better understanding of child’s condition
Promotes health literacy - helps child to understand about illness and treatment therefore child will be less frightened, better able to make informed decisions

91
Q

What is Piagets theory of childrens thinking stages

Young children

A

Age 18months - 6/7 years (pre operational)
Found confusion about causation of illness eg get a cold from trees so may view treatment or pain as a punishment
Usually define illness by its external signs eg heart attack is falling on your back

92
Q

What is piagets theory of children thinking (age 7-11)

A

More sophisticated understanding of causation but may be preoccupied by contamination eg germs
Still tend not to think about under the skin

Still difficulties with abstract reasoning eg implications for future
Eg concepts of health promotion

93
Q

What is piagets theory of childrens thinking age 11+

A

Formal operational thinking
Ability to reason about using abstract ideas
Useful for understanding the unobservable ie germs, DNA
Ability to start forming hypothesis (will be able to consider different treatment options)

94
Q

What is the role of ‘able instruction’

A

Vygotsky accepted piagets stage theory but argued that children could be helped to understand new information
The teacher provides scaffolding to allow child to build an existing understanding

95
Q

Examples of adverse pregnancy conditions or sub optimal intrauterine conditions

A

Poor maternal diet (low calorie/ low protein / high saturated fats)
Maternal stress (cortisol can cross placenta)
Hypoxia - smoking
Drugs / endocrine disrupting chemicals / alcohol abuse

96
Q

Consequences to placenta of sub optimal intrauterine conditions

A

Placental insufficiency: poor placental growth, poor transport mechanisms, impaired barrier properties, vascular dysfunction, aberrant invasion, increased cortisol secretion, growth factor secretions

97
Q

Consequences to offspring of sub optimal intrauterine conditions

A

Small baby and intra uterine growth restriction, metabolic changes, altered neurological development
Catch up growth in infants, obesity in children
Impaired glucose tolerance, insulin resistance, dyslipidemia, obesity, T2 diabetes, metbaolic syndrome when adult

98
Q

What is catch up growth

A

Small baby will try to catch up with growth when born but can then lead to obesity in childhood

99
Q

Reasons for low birth weight

A 
Preterm pregnancy 
Multiple pregnancy 
Placental insuffiency (maternal height) 
Genetics 
Sub optimal maternal environment
100
Q

What does IUGR stand for

A

Intrauterine growth restriction

101
Q

What does small for date mean

A

2 standard deviations below the expected weight at a particular gestational age using population growth centile charts

102
Q

Fetal physiology : oxygen and CO2

A

Fetus needs oxygen in relatively small continuous supply
Fetal stores of oxygen are very small
3kg fetus near term needs 18ml O2/min but stores 36ml, 2 mins worth of oxygen

103
Q

Difference between adult haemoglobin and fetal haemoglobin

A

Adult has 2 a and 2 B globin chains

Fetal has 2 alpha, 2 gamma globin chains. At any given time HbF has a higher affinity to and will bind more O2 than maternal Hb leading to high oxygen saturation of fetal blood

104
Q

When does the switch from HbF to HbA occur

A

Several months after birth

105
Q

What factors mitigate the fact that a fetus can only store 2 minutes worth of oxygen

A

Oxygen tension: PO2 in umbilical vein is low relative to PO2 in maternal blood so oxygen readily diffuses across placenta from mother to fetus

CO2 tension: CO2 from fetal metabolism diffuses back across the placenta as PCO2 is always higher in umbilical artery and vein compared to maternal blood

O2 saturation is always higher in fetal blood - 70%. Different O2 trapping property

106
Q

Describe the double Bohr effect as an oxygen trapping property of fetal blood

A

Uptake of fetal CO2 by maternal blood leads to a fall in the pH of maternal blood. This drives release of maternal O2
At the same time the rise in fetal pH due to removal of its CO2 facilitates uptake of O2

This facilitates transfer of extra 10% oxygen in the fetal direction

107
Q

Fetal response to maternal nutrition stress

A

There is a survival value for selecting genes that reduce fetal growth in response to maternal nutritional stress as a way of preparing the offspring for optimised survival in a resource poor world

108
Q

Role of placenta nutrient sensor

A

Can upregulate or downregulate transport of nutrients. Eg amino acid transport is down regulated prior to IUGR in rats fed a low protein diet

109
Q

What is the barker hypothesis

A

Lower the weight of the baby at birth and during infancy the higher the risk for coronary heart disease in later life

Other studies have shown that low birth weight is associated with increased risk of hypertension, stroke and T2 diabetes

110
Q

Define epigenetics

A

Mechanism of regulating gene expression, maintained across cell divisions without altering DNA sequence itself

111
Q

Define epigenome

A

The machinery that regulates gene expression and thus may alter phenotype

Gene silencing due to DNA methylation or histone modification

112
Q

How do epigenetic modifications to chromatin occur

A

1) DNA methylation
2) histone modification
3) chromatin remodelling through non coding RNAs

113
Q

Describe DNA methylation

A

Addition of a methyl group to a cytosine residue on a cytosine-guanine dinucleotide. In mammals nearly all DNA coding for genes have methylated CpG dinucleotides

114
Q

Describe histone modification

A

Binding of acetyl or methyl groups to histone tails altering wrapping of DNA

115
Q

When can epigenetic modifications occur

A

1) epigenetic reprogramming during gametogenesis
Behind uniparental imprinting of alleles. Genes affected by epigenetic changes in the spermatogenic lineage differ from those imprinted in the oogenetic lineage

2) epigenetics in early development: important dpi-genetic processes can occur during development in the periconceptual period
3) epigenetics after fertilisation: upon fertilisation there is rapid demethylation of the entire parental genome in all genes. However some genes remain imprinted (1% of genes in the genome)

116
Q

Epigenetic mechanisms can be modulated throughout life

A

Twin studies: monozygotic twins with different environmental exposures resulting in different phenotypes regardless of identical genomes

117
Q

Roles of growth factors

A

Insulin like growth factors 1 and 2 are produced by fetal cells (inc placenta) synthesis of both rise with pregnancy (IGF2 is 2-3 fold higher)

IGF1- production is reposnsive to nutrient levels, declining when nutrients fall. It is sensitive to insulin, thyroxine, glucocorticoids (matching fetal growth to nutrient supply)

IGF2 stimulates placental growth and transport mechanisms - optimal transplacental transport of nutrients is essential for fetal growth

118
Q

Why is IGF2 a paternally expressed gene

A

Argued to result from males dominating an evolutionary conflict controlling the extent of resources which are extracted from the mother
Expression of fathers allele in humans favours a bigger baby where’s expression of mothers allele favours a smaller child

119
Q

Define altruism

A

A behaviour benefitting another individual which incurs a direct cost for the individual performing the altruistic action

120
Q

Purpose of antenatal care

A

Used to detect early signs of complications, followed by a timely intervention if any found

Focuses on educating the pregnant woman on a range of topics including wellbeing, birth preparedness, complication readiness and breastfeeding

121
Q

What is the neural tube

A

The embryonic precursor to the central nervous system
Closed by day 28 (4th week)

Folic acid supplements reduces the risk of neural tube defects

122
Q

Vitamin D supplementation in pregnancy

A

10 mcg daily in high risk groups

Needed for our bowel to absorb sufficient quantities of phosphate and calcium
Essential for adequate bone mineralisation

Deficiency results in rickets in children and osteomalacia in adults, neonatal tetany

123
Q

What are the different screening tests done before 10 weeks

A

Sickle cell anaemia and thalassaemia

124
Q

What are the screening tests done at 8-10 weeks

A

HIV
Hep B
Syphilis

Blood group and rhesus status

125
Q

What are the screening tests done at 11-14 weeks

A

Downs
Edwards
Patau’s

126
Q

What happens if an Rh- mother is carrying a Rh + fetus

A

Father is Rh+

Rh antigens from developing fetus can enter the mothers blood during delivery
The mother will produce anti Rh antibodies
If the woman becomes pregnant with another Rh+ fetus her anti Rh antibodies will cross the placenta and damage fetal red blood cells

127
Q

How is rhesus disease prevented

A

15% of population are rhesus negative

Prevent rhesus disease by giving the mother anti Rh immunoglobulin
Without this 16% of women become sensitised

128
Q

Screening for trisomies (presence of an extra chromosome)

A

Combined test 10-14 weeks
Blood test and an ultrasound to measure nuchal translucency

Diagnostic test: amniocentesis (from 15 weeks)
Chorionic villus sampling (11-14 weeks)

129
Q

How does non invasive prenatal testing (NIPT) for trisomies work

A

Works by analysing the DNA fragments in the maternal blood during pregnancy = cell free dna

Most comes from the mother but around 10-20% of it comes from the placenta which is representative of the unborn baby (cell free fetal DNA)

130
Q

Screening for HIV

A

Universal HIV screening introduced in 1999- 97% uptake
1200 women per year in UK

Risk of mother to child transmission with undiagnosed = 25%
Risk with diagnosed HIV and appropriate management = 0.27%

1) viral suppression (combination anti retro viral therapy)
2) mode of delivery (C section)
3) not breastfeeding
4) ART for neonate

131
Q

Screening for syphilis

A

Universal antenatal syphilis screening 97% uptake
Congenital syphilis almost entirely preventable
Single dose of IM penicillin

132
Q

Risk of smoking during pregnancy

A

11% of pregnant women in UK smoke at the time of giving birth

Increases vascular resistance in the placenta and impairs oxygen exchange
Causes up to 2200 premature births, 5000 miscarriages and 300 perinatal deaths every year in UK

Fetus more likely to have low birth weight, ENT problems, respiratory conditions, obesity or diabetes

133
Q

Complications of pre eclampsia

A

Maternal: fits, HELLP syndrome (rare liver and blood clotting disorder), stroke, liver failure, renal failure, pulmonary oedema

Fetal: fetal growth restriction, stillbirth, prematurity

134
Q

High risk factors for pre eclampsia

A

Hypertensive disease in a previous pregnancy

Chronic kidney disease

Autoimmune disease such as systemic lupus erythematosus or antiphospholipid syndrome

T1 or T2 diabetes

Chronic hypertension

135
Q

Moderate risk factors for pre eclampsia

A

First pregnancy

Age 40+

Pregnancy interval of more than 10 years

BMI of 35kg/m2 or more at first visit

Family history of pre eclampsia

Multiple pregnancy

136
Q

Prevention of pre eclampsia

A

Low dose aspirin

75mg daily

137
Q

What is gestational diabetes

A

Diabetes that occurs during pregnancy and disappears after giving birth

5% of all pregnant women

Screen high risk groups at 28 weeks with an oral glucose tolerance test

Majority of women treated with dietary changes

10% of women require metformin and / or insulin

138
Q

Complications of gestational diabetes

A

Maternal: pre eclampsia; polyhydramnios; prolonged labour, obstructed labour; Caesarean section; uterine atony; postpartum haemorrhage

Fetal: congenital abnormalities; fetal macrosomia; stillbirth; birth injuries ; neonatal hypoglycaemia

139
Q

What is fetal growth restriction

A

3% of all pregnancies

Condition in which fetus’ growth slows or stops during pregnancy
Majority of cases due to placental dysfunction

140
Q

Benefit of folic acid supplementation

A

Reduces risk of neural tube defects

141
Q

Benefit of vitamin D supplementation

A

Deficiency results in rickets (children) and osteomalacia (adults), neonatal tetany

142
Q

Define intrauterine growth restriction (IUGR)

A

Birth weight <2.5kg

143
Q

Define macrosomia

A

Birth weight > 4kg

144
Q

Changes in carbohydrate metabolism in normal pregnancy

A

Foetus uses glucose, lower fasting maternal blood glucose

Insulin resistance increases with gestation, peripheral insulin resistance due to hormones

Diabetes occurs if B cells of pancreas are unable to produce sufficient insulin to prevent hyperglycaemia

145
Q

List potential neonatal complications (diabetes)

A 
Respiratory distress syndrome 
Polycythaemia 
Hyperbilirubinaemia and jaundice 
Hypoglycaemia 
Hypocalcaemia 
Hypomagnesaemia 
Hypothermia 
Cardiomegaly 
Birth trauma 
Delayed gastric emptying
146
Q

Why is the risk of macrosomia higher due to diabetes mellitus

A

High maternal blood glucose crosses the placenta and stimulates foetal insulin production which acts as a growth promoter

Excess glucose laid down as glycogen in the liver and adipose tissue

147
Q

Postnatal care for patients presenting with diabetes mellitus

A

Stop all hypoglycaemics, return to pre pregnnacy medication

Less tight glycaemic control

Encourage breastfeeding

148
Q

Other maternal complications of diabetes

A

Hypoglycaemia
Retinopathy
Nephropathy
Cardiac disease

149
Q

Define essential hypertension in pregnancy

A

Increase of 30/+ systolic mmHg or 15/+ diastolic mmHg

150
Q

Indications for delivery in pre eclampsia

A

Hypertension remaining uncontrolled despite maximal anti-hypertensives

Eclampsia

Renal, hepatic or coagulation impairment

Pulmonary oedema

Foetal distress

Milder pre eclampsia at term

151
Q

Maternal hepatic complications of pre eclampsia

A

Hepatocellular dysfunction

Ischaemic pain

Subcapsular haemorrhage

Liver rupture

152
Q

Define severe hypertension

A

BP >160/110 mmHg on 2 occasions, 6 hours place

153
Q

Define hypertension

A

BP >140/90 mmHG on 2 occasions, 6 hours place

154
Q

Define significant proteinuria

A

> 300mg protein in a 24 hour urine collection or >30mg/mL in a spot urinary protein: creatinine sample

155
Q

Different types of hypertension in pregnancy

A

Chronic: present at booking / before 20 weeks, no proteinuria

Gestational, present after 20 weeks, no proteinuria

Pre-eclampsia, present after 20 weeks, significant proteinuria

156
Q

4 pathophysiological mechanisms in pre eclampsia

A

Abnormal placentation

Endothelial cell dysfunction

Organ hypoperfusion

Plasma volume loss

157
Q

Which hormone is released after ovulation occurs and can be used as a marker of fertility

A

Progesterone as it is a sign that an egg is being released

158
Q

What is haemodilution

A

Occurs in pregnancy because plasma volume increases by 50% and RBC increases by only 20% so even though maternal blood volume increases by 30% the ratio of plasma to RBC is unmatched

159
Q

What are the key pointers of placental abruption

A

Age (increase in risk with age)
High parity (>5 pregnancies, >25 weeks gestation)
Onset of clincial shock
Tender, hard uterus on examination

160
Q

Presenting symptoms of placental praevia

A

Painless vaginal bleeding

Med 3 (10 decks)

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