Pregnancy Flashcards
What is an ectopic pregnancy?
Implantation of a fertilised egg at a site outside the uterus
Most commonly occurs in the ampulla of the Fallopian tube (~80%)
—> rupture of Fallopian tube —> haemorrhage —> peritonitis
Can also occur:
- interstitial (~2%-5%)
- cervix
- peritoneum
- abdominal viscera
- in the pouch of Douglas
Pain felt in lower abdominal quadrants (stretching/tearing of peritoneum) —> right iliac fossa (often misdiagnosed as appendicitis)
Haemorrhage into peritoneum —> diaphragmatic irritation —> referred shoulder tip pain
More dangerous when it occurs in the isthmus/intramural Fallopian tube as less space is available for the embryo to grow before the tube is ruptured (thick muscularis mucosa is inflexible)
note: blood passing from vagina is usually withdrawal bleeding, not due to bleeding at the site of rupture (caused by reduction in hCG —> corpus luteum not maintained)
What is the clinical presentation of pain in ectopic pregnancy?
(assuming in ampulla of uterine tube)
Before rupture = lower abdominal quadrants due to stretching/tearing of peritoneum
(hence commonly misdiagnosed as appendicitis)
Rupture —> haemorrhage into peritoneum —> diaphragmatic irritation —> referred pain to tip of shoulder (phrenic nerve - dermatomes C3, C4, C5)
note: blood passing from vagina usually withdrawal bleeding caused by fall in hCG (not due to bleeding at site of rupture)
What can be torn during childbirth, and what are the consequences?
Levator ani muscles:
- pubococcygeus —> prolapse/herniation of bladder/urethra —> incontinence
- medial part of pubo-rectalis (inserts into perineal body) —> herniation of rectum (tear extending into external anal sphincter) —> difficulty with defecation/faecal incontinence
What is an episiotomy? What needs to be repaired and checked as a result?
Incision of skin in perineum to allow passage of the head of the foetus through the vagina and prevent damage to perineal body
note: additionally, incision is easier to suture than a tear
note: median episiotomy divides the perineal body; has since been abandoned in favour of a postero-lateral episiotomy
Repair:
- vaginal mucosa and submucosa
- perineal skin
- muscles & fascia of perineum
Perform a vaginal exam and a rectal exam after repairing
What cells of the conceptus go on to form the placenta?
Syncytiotrophoblast = forms placenta; invades endometrium; multi-nucleated (no interstitium, therefore very short diffusion pathway)
+ cytotrophoblast = stem cell layer responsible for growth & repair of syncytiotrophoblast and implantation
Outline the development of the placenta.
Week 5:
Primitive villi all over chorion (recede over time except for one zone —> placenta)
Amniotic sac enlarges, yolk sac disappears
Week 12:
Chorion loses villi away from decidua basalis (placenta)
Week 22:
Amniochorionic membrane fuses to decidua parietalis
note: 1st trimester = placental barrier composed of syncytiotrophoblast, cytotrophoblast, connective tissue, & foetal capillaries
3rd trimester = placental barrier only composed of syncytiotrophoblast & foetal capillary endothelium
How does the embryo implant in the uterus? How does this change as the foetus develops?
Uterine epithelium breached & conceptus implants in stroma
1st trimester placenta:
- placental “barrier” relatively leaky & thick
- complete cytotrophoblast layer beneath syncytiotrophoblast
3rd trimester placenta:
- increased s.a. for exchange
- placental “barrier” now thinner (as needs of foetus increases)
- cytotrophoblast layer beneath syncytiotrophoblast is lost
- placenta is haemomonochorial (single layer of trophoblast separates maternal blood from foetal capillaries - optimises transport)
What are the aims of implantation?
Establish basic unit of exchange: Primary villi (differentiate) ---> Secondary villi (invades mesenchyme core) ---> Tertiary villi/chorionic villi (invasion of mesenchyme core by foetal vessels which differentiate from mesenchyme)
Anchoring of placenta: establishment of outermost cytotrophoblast shell (cytotrophoblast migrates through villi to be outside placenta)
Establish maternal blood flor within the placenta: chorionic villi bathed in maternal blood to optimise transport
How does implantation of an embryo modify the histology of the endometrium?
Pre-decidual cells (cells shed during menstruation) modified to form decidua (balancing force for invasion of trophoblast)
- decidua basalis = maternal portion of placenta which induces the trophoblast to form chorionic villi
- decidua capsularis = tissue separating the lumen of the uterus from the embryo —> chorion laeve
- decidua parietalis = endometrial tissue between the uterine lumen and the myometrium
Remodelling of spiral arteries —> creates low resistance vascular bed to maintain high flow required for high foetal demand (particularly in late gestation)
note: extra-villus trophoblasts line maternal blood vessels, therefore maternal cells are directly adjacent to foetal cells
When does incomplete invasion of the endometrium by the embryo occur?
Placental insufficiency —> intra-uterine growth restriction
Pre-eclampsia —> intra-uterine growth restriction, maternal symptoms (hypertension, proteinuria) + problem with remodelling of spiral arteries
What is a cotyledon, and what is it composed of?
Compartment of placenta containing a major branch of the umbilical blood vessels - group of chorionic villi bathed in maternal blood
Maternal portion:
- cytotrophoblastic shell
- maternal vein & artery —> form blood pools adjacent to chorionic villi
Foetal portion:
- chorionic villi containing foetal capillaries
- one umbilical vein (oxygenated) & two umbilical arteries (deoxygenated)
note: normally the placenta is vasodilated (expanded) but in pre-eclampsia the placenta is vasoconstricted (contracted; due to poor uteroplacental circulation & widespread endothelial dysfunction)
What are the functions of the placenta?
Synthesis of: - glycogen - cholesterol ---> steroid hormones - fatty acids (for support of mother, not foetus)
Production of hormones:
- protein hormones = hCG, somatomammotrophin/thyrotrophin/corticotrophin
- steroid hormones = progesterone & oestrogen
(placenta produces enough progesterone to maintain pregnancy without progesterone from corpus luteum until the end of the 1st trimester)
Transport:
- simple diffusion (water, electrolytes, urea, gases) - dependent on uteroplacental circulation
- facilitated diffusion (glucose)
- active transport (amino acids, iron, vitamins)
- receptor-mediated (IgG - passive immunity)
What is hCG?
Human chorionic gonadotrophin
Protein hormone produced in 1st months of pregnancy by cells of fertilised ovum
Supports the secretory function of the corpus luteum —> increased secretion of progesterone & oestogen —> endometrium maintained
Produced by syncytiotrophoblast (therefore pregnancy-specific)
note: indicative of trophoblast diseases e.g. hydratidiform mole/molar pregnancy = pregnancy without embryo (abnormal independent production of trophoblast), choriocarcinoma = malignant version of trophoblast
Give some examples of the effects of pregnancy on the mother by pregnancy-related hormones.
Human chorionic somatomammotrophin & human placental lactogen cause slight insulin resistance in mother —> increases glucose available to foetus (+ risk of gestational diabetes)
Progesterone increases maternal appetite to increase fat stores in preparation for larger foetuses
Increased calcium release from maternal bones to supply foetus with calcium (can cause dental caries/osteopenia)
What is the purpose of maternal blood lakes in the placenta?
Compensates for compression of blood vessels during labour causing reduced uteroplacental circulation
~300ml
Give some examples of infections and teratogens which can cross the placenta.
Infections:
- Varicella zoster (chickenpox/shingles)
- Cytomegalovirus (herpes)
- Treponema pallidum (syphilis)
- Toxoplasma gondii (toxoplasmosis)
- Rubella (causes miscarriage or congenital rubella syndrome = sensorineural deafness, eye abnormalities, congenital heart disease, etc.)
Teratogens:
- thalidomide
- alcohol
- anti-convulsants
Explain the importance of D antibodies in pregnancy.
Rhesus positive = D antigens present on RBCs
Rhesus negative = anti-D antibodies produced (inc. against IgG)
If mother is Rhesus negative and their foetus is Rhesus positive, they will produce anti-D antibodies after their first pregnancy (sensitisation) —> next pregnancy the anti-D antibodies will attack the foetus —> haemolysis (reticulocytosis, anaemia, hydrops fetalis)
Therefore Rhesus negative first time mothers are offered prophylactic anti-D IgG to remove foetal Rhesus positive RBCs —> no sensitisation occurs
Kleihauer test demonstrates presence/absence of foetal cells in maternal circulation
What conditions are screened for at antenatal screenings?
H&E = risk factors e.g. for gestational diabetes
Blood test = Rhesus status, ABO blood type, Hb level, ?infection
Urinalysis = ?proteinuria (indicates pre-eclampsia)
What maternal cardiovascular changes occur during pregnancy?
- increased blood volume —> dilutional anaemia
- increased stroke volume —> increased bpm (to 80-90bpm) & cardiac output (by 40%) —> auscultatory changes (flow murmurs)
- reduced systemic vascular resistance (due to progesterone) —> initial fall in BP (trimesters 1 & 2; can mask pre-existing hypertension, cause sweating easily, nasal congestion, “feeling the heat”) —> increase in BP (trimester 3) due to aortocaval compression by gravid uterus (increased risk of impaired utero-placental circulation when supine; therefore women encouraged to lie on left-hand side)
- venous distension (smooth muscle relaxation effect of progesterone + pressure of uterus on IVC when recumbent) —> varicose veins & haemorrhoids
- upward displacement & hypertrophy of heart
note: normally systolic BP NEVER increases in pregnancy
note: mean BP remains the same (increased stroke volume causes a slight increase in systolic BP and a slight decrease in diastolic BP)
note: when supine, the uterus compresses the IVC —> reduced venous return —> reduced diastolic pressure —> hypotension
What maternal urinary changes occur during pregnancy? Why are these changes necessary? …………
- increased intra-ureteral tone
- increased GFR (50%-60%) —> reduced functional renal reserve
- increased renal plasma flow (to a greater degree than GFR increase) —> reduced filtration fraction in trimesters 1 & 2
- increased creatinine clearance (therefore lower creatinine)
- increased protein clearance (therefore lower protein)
- reduced urea
- reduced bicarbonate
- increased risk of urinary incontinence (bladder compressed by gravid uterus/when foetal head is engaged towards the end of pregnancy)
note: progesterone causes dilation of ureters (slows urine excretion —> increased risk of UTIs) —> hydroureter —> hydronephosis
note: gravid uterus can compress the ureters/bladder —> urinary stasis —> risk of UTIs —> risk of pyelonephritis —> pre-term labour
note: ‘normal’ kidney function actually reflects decreased kidney function when pregnant
What maternal respiratory changes occur during pregnancy?
- displacement of diaphragm & increase in AP/transverse diameters (flaring of lower ribs) —> decreased functional residual capacity (but balanced by expiratory reserve volume)
- widening of intercostal angle
- increased alveolar/minute ventilation & increased tidal volume (by 40%) (no change in resp. rate)
- increased risk of metabolic acidosis (reduced buffer capacity, increased resp. drive by progesterone —> resp. alkalosis —> increased bicarbonate excretion)
- increased oxygen consumption (by 15%)
What maternal metabolic changes occur during pregnancy?
Carbohydrates:
- increased maternal insulin resistance (due to hPL, glucose, oestrogen, progesterone, cortisol) —> switch to gluconeogenesis & lipolysis
- reduced fasting blood glucose
- increased post-prandial (post-meal) blood glucose
Lipids:
- increased synthesis of lipids in trimester 1
- increased lipolysis in trimesters 2 & 3
- increased metabolism of peripheral fatty acids in late pregnancy
- increased free fatty acids & ketones on fasting (so glucose is available for foetus) (increased risk of diabetic ketoacidosis)
Thyroid:
- increased TBG production
- increased T3 & T4 production (but free T4 normal)
note: hCG directly stimulates thyroid, therefore TSH levels can be decreased due to negative feedback
Calcium:
- increased uptake of dietary calcium from maternal gut
- increased secretion of PTH in third trimester —> increased release of calcium from bone (risk of osteoporosis/dental caries; therefore expectant mothers should increase dietary calcium intake by ~70%)
+ increased prolactin release by oestrogen
What is gestational diabetes?
Carbohydrate intolerance first recognised in pregnancy and not persisting after delivery (diagnose via oral glucose tolerance test)
Risk factors:
- previous history
- increased age
- increased weight
- history of babies which where large for gestational age
Poor control:
- risk of macrosomic (large) foetuses (increased insulin secretion in foetus —> glucose stored as fat)
- stillbirth
- congenital defects (esp. if maternal hyperglycaemia occurs during period of development)
- prematurity
- impaired maturation
- resp. disorders of the newborn
Macrosomic foetuses are difficult to deliver due to their large size
Once born the foetus has reflex hypoglycaemia due to high levels of circulating insulin (brain at risk)
What maternal gastro-intestinal changes occur during pregnancy?
- change in disposition of viscera by uterus e.g. appendix moved to RUQ
- progesterone causes smooth muscle relaxation —> delayed gastric emptying (heartburn & constipation), stasis in biliary tract (increased risk of cholecystitis & pancreatitis - also increased risk due to hyperlipidaemia)
What maternal haematological changes occur during pregnancy?
- increased fibrin deposition at implantation site
- increased fibrinogen & clotting factors
- reduced fibrinolysis
- stasis of blood & venodilatation
- increased plasma volume & RBC mass (but discrepancy exists —> apparent fall in maternal Hb —> dilutional/physiological anaemia
- reduced IgA, IgG, & IgM (prevents rejection of foetus by mother; but mother more vulnerable to viral infections)
note: above all increase the risk of thromboembolic disease (but warfarin is teratogenic to the foetus)
note: iron/folate deficiency-causing anaemia can still occur
note: foetus can acquire maternal autoimmune conditions due to the transfer of antibodies e.g. Graves’ disease, Hashimoto’s thyroiditis
What is the effect of smoking and alcohol on the foetus?
Maternal smoking:
- reduced placental blood flow & growth
- reduced foetal nutrition —> reduced birth weight (by ~200g)
- CO shifts maternal Hb-O2 curve to the left —> reduced pO2 available for foetus
Maternal alcohol misuse: foetal alcohol syndrome = low birth weight, potential mental retardation, potential head & facial abnormalities
What hormone can be measured in the maternal blood which can indicate foetal progress?
Oestriol (E3)
Oestriol produced by placenta from 16-OH DHEAS
DHEAS converted to 16-OH DHEAS in the foetal liver
Therefore oestriol is dependent on foetal liver & adrenal metabolism as well as placental function —> low levels can indicate foetal distress
How are multiple concurrent pregnancies prevented? ????
Inhibin inhibits FSH —> no further follicular development
Inhibin inhibits LH —> no further ovulation
+++??? + cervical mucus plug
What are the symptoms of anaemia during pregnancy? How is this treated?
More iron required in pregnancy due to expanded volume of the blood (despite menstrual cycles ceased)
Maternal symptoms:
- asymptomatic
- fatigue
- breathlessness
- increased risk of mortality
Foetal symptoms:
- foetal growth retardation
- increased risk of stillbirth
Treatment = oral iron sulfate/gluconate
What is pre-eclampsia? What is eclampsia?
Pre-eclampsia = combination of pregnancy-induced hypertension and proteinuria, with or without oedema (oedema is common in pregnancy, but a sudden increase, esp. in facial oedema, can indicate pre-eclampsia)
Severe S&S:
- increased diastolic BP
- persistent/worsening albuminuria
- oliguria
- thrombocytopenia
- increased liver enzymes
- lack of foetal growth
- oligohydramnios
- pulmonary oedema
- headache
- visual complaints
Assess by measuring BP, examining for oedema, examining optic fundi (potential for CNS involvement), examining tendon reflexes (hyperreflexia is an indication of worsening vasospasm on CNS function), checking foetal size & heart sounds
Eclampsia = onset of convulsions in a pregnancy complicated by pre-eclampsia
What are some complications associated with multiple pregnancies?
Increased incidence of:
- pregnancy-induced hypertension
- anaemia
- polyhydramnios
- preterm labour
- perinatal mortality
- antepartum haemorrhage
Give some examples of factors which affect foetal growth.
- maternal habits e.g. smoking, alcohol
- maternal parity (how many previous births the mother has had)
- efficiency of placenta
- umbilical/placental blood flow
- genetic factors
- maternal race, height, and weight
How can uteroplacental or foetoplacental circulations be assessed?
Doppler ultrasound
What is measured at the ultrasound scan at 20 weeks? Why is this done at 20 weeks?
Measurements confirm earlier dating estimations and provide a reference point for later investigations
Functions:
- presence/absence of intrauterine pregnancy/ectopic pregnancy
- determine gestational age & measure foetal growth e.g. abdominal circumference (glycogen storage in liver & amount of sub-cutaneous fat), biparietal diameter, crown-rump length, femur length, head circumference
- measurement of amniotic fluid
- identify maternal pelvic abnormalities
- guide needle for amniocentesis
- estimate foetal weight
- identify multiple pregnancies
- detect foetal abnormalities e.g. neural tube defects
- detect placental abnormalities e.g. placenta praevia
Done at 20 weeks because:
- organs can now be visualised
- if anomalies are seen, it is still early enough to consider intervention/termination
- ultrasound dating becomes less accurate as pregnancy proceeds
note: mother should be aware of foetal movements by 20 weeks (“quickening”); multiparous women may detect them earlier
What is a transvaginal ultrasound at 8 weeks used for?
8 weeks = uterus still in pelvis, hence abdominal ultrasound cannot be used
- detect foetal cardiac activity
- exclude causes of early loss of foetus e.g. anembryonic gestation (blighted ovum)
- exclude ectopic pregnancy
Why are folic acid supplements recommended for pregnant women?
Folate is important for synthesis/repair/methylation of DNA, aiding rapid cell division/growth, production of RBCs
Helps prevent neural tube abnormalities
What can levels of alpha-fetoprotein in pregnant women indicate?
Measure at 15-19 weeks
Elevated levels can indicate:
- multiple pregnancy
- open neural tube defect —> ultrasound study +/- amniocentesis
When can the foetal heartbeat be detected with a Doppler stethoscope and with an ordinary stethoscope? What is the advantage of using a scalp electrode to measure foetal heart rate?
10-12 weeks - Doppler stethoscope
18-20 weeks - ordinary stethoscope
Scalp electrode allows continuous close monitoring of foetal heart rate regardless of maternal position
What is the average foetal heart rate at term? How does the foetal heart rate usually change with foetal movements?
140-160bpm
3 or more foetal movements should be accompanied by a rise in foetal heart rate
note: repeat this test if no foetal movement of change in heart rate is detected, as the foetus may be sleeping
When are foetal respiratory movements evident by sonography?
12 weeks
note: at 36 weeks there are irregular bursts of resp. movement (rates up to 40-60/min) with periods of apnoea (including hiccups)
note: resp. movements are diaphragmatic —> movement of amniotic fluid into and out of the lungs
When does foetal surfactant production begin? Why is this significant?
Starts at 20 weeks, increases dramatically after 30 weeks, significant levels at 34 weeks
Needed to prevent alveolar collapse & allow efficient gas exchange
Premature babies at increased risk of respiratory distress syndrome due to lack of surfactant (treat by giving mother steroids to accelerate production of surfactant before delivery)
How is symphysis-fundal height used to monitor a pregnancy? What does this depend on?
12 weeks = uterus is palpable above the pubic symphysis
Height from top of symphysis to top of fundus of the uterus (cm) = no. of weeks gestation
Depends on no. of foetuses, volume of amniotic fluid, and the extent of engagement of the head and lie of the foetus
note: can also measure the height of the fundus of the uterus in relation to other structures too e.g. umbilicus, xiphisternum
note: lag of 4cm+ in fundal height is suggestive of intrauterine growth restriction/foetal growth restriction
What are the different types of intra-uterine growth restriction?
Type 1 (symmetric) = growth inhibition occurring early in pregnancy
e.g. TORCH, chromosomal disorders, congenital malformations
Type 2 (asymmetric) = restriction of nutrient supply in utero (brain sparing but abdominal organ growth slowed due to reduction in foetal cardiac output) due to poor maternal nutrition or decline in nutrient delivery to the foetus (in the 3rd trimester)
e.g. chronic hypertension, renal disease
What is TORCH syndrome?
Group of vertically transmitted infections
Toxoplasma gondii (toxoplasmosis) Other Rubella Cytomegalovirus Herpes simplex
Complications: - stillbirth - miscarriage - delayed foetal growth & maturation - lethargy - fever - difficulties feeding - hepatomegaly - anaemia - petachiae/purpura - jaundice etc.
What is oligohydramnios?
Decrease in amount amniotic fluid surrounding foetus
Oligohydramnios associated with nutritional deprivation/utero-placental insufficiency which causes reduction in foetal urine production
Causes:
- idiopathic
- placental insufficiency
- foetal kidney malfunction
- maternal hypertensive disorders
- premature rupture of membranes
- foetal bladder outlet obstruction
- premature leakage of amniotic fluid
How is amniotic fluid produced? What is its function?
Amniotic fluid is a dialysate of maternal & foetal fluid
Prior to week 8 = amniotic fluid produced by transudation of fluid across the amnion & foetal skin
Week 10 = foetal urine first produced (kidney function begins)
note: foetal lungs also contribute to amniotic fluid
Swallowed & digested by the foetus (equal rate to production)
Foetus makes intermittent breathing movements in latter part of gestation (conditioning of respiratory muscles) which flushes the lungs with amniotic fluid (keeps airways clean & patent)
Provides mechanical protection of moist environment (foetal skin is non-keratinised so it would lose a lot of O2 if exposed to air)
8 weeks = ~10ml, 38 weeks = ~1l, 42 weeks = ~300ml
Early pregnancy = formed from maternal fluids & foetal extracellular fluids
Late pregnancy = turnover via foetus
What is polyhydramnios?
Increase in amount of amniotic fluid surrounding foetus
Causes:
- diaphragmatic hernias
- oesophageal/duodenal atresia
- anencephaly (partial/complete absence of bones/meninges/brain in the rear of the skull)
- inencephaly (defect in occipital bone + spina bifida of cervical vertebrae + retroflexion of head on cervical spine)
- hydrocephaly (abnormal increase in CSF within the ventricles of the brain)
- maternal diabetes
- multiple pregnancy
- placental abnormality
Give some examples of cases when the foetus is considered at-risk.
- maternal hypertension
- maternal heart/liver disease
- multiple gestation
- maternal diabetes
- evidence of foetal growth retardation
- suspected oligohydramnios
- presence of placental abnormality
- post-date pregnancy
What is meconium? What does it indicate?
First stool(s) of newborn baby
Green, dark, sticky appearance
Composed of cellular debris, mucus, & bile pigments
Formed from digestion products of amniotic fluid the foetus has swallowed
Indicates episode of foetal distress
Describe the oxygen supply to the foetus.
- increase in maternal pO2 (hyperventilation stimulated by progesterone) to increase diffusion gradient
- foetal Hb saturated at lower partial pressure of oxygen, does not respond to 2,3-BPG, and foetus has more Hb present overall
- low diffusion resistance across placenta
- double Bohr effect: CO2 moves from foetus to mother —> acidifies maternal blood —> O2 more likely to be released from maternal Hb; maternal pCO2 is lower
- oxygen transport rate determined by umbilical artery pO2
note: little myoglobin in foetus due to less blood overall, less saturated Hb, and less muscle —> less O2 stores (can only survive without O2 for ~2min)
Why is it important for CO2 to be transported from the foetus to the mother?
Foetus cannot expire CO2
Kidneys in foetus are non-functioning so HCO3- cannot be used to buffer increased CO2
How is the foetal circulation adapted? Why are these adaptations required?
Left umbilical vein (70% sat.) —> ductus venosus —> IVC (65% sat.) —> foramen ovale —> pulmonary venous flow (60% sat.) & left atrium & ventricle
Right ventricle —> pulmonary artery —> ductus arteriosus —> aorta (distal to supply to the head) —> umbilical artery —> body, gut, & placenta
Required as umbilical venous blood is effectively delivered to the hepatic portal vein, so without adaptations O2 would be lost in the liver, mix with deoxygenated venous blood from the IVC and SVC into the right atrium, and be lost in the non-functioning lungs.
Why may babies be born slightly jaundiced?
In utero the foetus cannot conjugate bilirubin, it must pass it to the mother to be conjugated and excreted
At birth conjugation is established in the foetal liver when the baby is exposed to light
If this does not happen quickly enough, the baby may become jaundiced
Is a constant foetal heart rate a good sign? When is the definitive foetal heart rate achieved?
No - foetuses have daily rhythms of heart rate, breathing, and activity.
Heart rate variability is a good index of developing control systems
15 weeks - definitive heart rate formed
note: foetal bradycardia is associated with foetal mortality
Reminder: what occurs during the foetal period of development?
Growth & physiological maturation of structures created during the embryonic period (preparation for transition to independent life after birth)
What is crown-rump length?
Measurement from foetal crown to foetal rump in weeks 7-13
Dates pregnancy —> estimated delivery date
Assessed via ultrasound scan in T1 (also used to check location, number, and viability of foetus + check foetal heartbeat)
9 weeks = head is 50% of CRL but subsequently the body lengthens and lower limb growth accelerates
How is foetal wellbeing assessed antenatally?
Foetal movements (20 weeks)
Uterine expansion (once uterus has moved into the abdomen); measured by symphysis-fundal height
Ultrasound scan:
- no. of foetuses
- exclude ectopic pregnancy
- assess foetal growth (compare to predicted growth to determine gestational age)
- foetal abnormalities e.g. heart septation, spinal cord & vertebrae
note: 3 or 4-D ultrasound can be used to detect facial abnormalities
How is foetal age estimated?
Last menstrual period (LMP); inaccurate due to variations in cycle length, implantation bleeding being mistaken for LMP, LMP forgotten
Crown-rump length
Abdominal circumference
Femur length
Bi parietal diameter (T2-T3) = distance between parietal bones
Outline the development of the nervous system in the foetus.
First to begin & last to finish
8th week = practising for postnatal life e.g. suckling, breathing
17 week+ = maternal awareness of foetal movements (quickening)
4th month = corticospinal tracts begin to form (required for coordinated voluntary movements)
9th month = myelination of brain begins (hence infant cannot walk until 1st year onwards)
What effect might relaxin cause during late pregnancy?
Lordosis
Relaxation of vertebral ligaments and additional weight of the foetus
What hormone is responsible for the feelings of heartburn, constipation, and “feeling the heat” during pregnancy?
Progesterone
