REPRO - Pregnancy Flashcards
What are the 2 main factors responsible for maternal changes in pregnancy?
- high levels of steroids
- mechanical displacement and foetal demands
What are decidual cells filled with. They cover the uterus surface pre-decidualisation..what do the cells become if pregnancy ensues?
They are filled with lipids and glycogen and become the maternal part of the placenta
Lysing of which layer is necessary for the trophoblast and decidua to contact and fuse into synctiotrophoblast?
Zona pellucida
Name an autocrine GF for the blastocyst secreted by the synctiotrophoblast from week 4. Function?
Human chorionic gonadotropin
Rescues CL so endometrium not shed and CL makes more steroids
Human Placental Lactogen (hPL) has anti-insulin effect mimicking which hormone
GH
Progesterone causes SM relaxation and breast development. What do oestrogens cause in pregnancy?
- uterine hyper trophy
- insulin resistance
- more clotting factors
- breast development
Why does energy output increase in pregnancy?
- more respiration effort and CO
- need to store energy for foetus, labour and postnatally
What changes to BMR occur in pregnancy, mid gestation vs late gestation?
- increases by 350kcal/day in mid gestation
- by 250kcal/day in late gestation
1st trimester fasting serum glucose is low, as pancreatic cells increase in number so circulating insulin is high, maternal reserves are made. What happens in 2nd trimester?
- placental lactogen (hPL) causes insulin resistance so less glucose in stores, more in serum so more crosses placenta
- foetal reserves
About 8.5l water are gained in pregnancy, plasma volume increases 40%. Name 3 reasons/mechanisms this occurs?
- E2&progesterone act like mineralocorticoids on the RAAS system so more Na+ retained
- placental Renin is released
- E2 upregulates angiotensinogen synthesis in liver so more Ang II and RAAS
- lower thirst threshold so drink more
What 3 maternal changes occur to respiration in pregnancy?
- more sensitive to hypercapnia so breathe deeper
- minute volume decreases by 40%
- high arterial O2, low PCO2 to facilitate gas transfer
- thoracic anatomy changes, ribs displaces up
Maternal blood red cell mass increases by 18% in pregnancy but plasma vol has increased by 40%..what is this called?
Physiological haemodilution (not anaemia) NB: maternal gut is more efficient at absorbing iron
What change in maternal blood for placental separation increases risk of DVT in pregnancy?
-more leukocytes, clotting factors and fibrinogen make the blood hypercoaguable
What is the risk with smoking in pregnancy?
-increases carboxy-HB in mothers blood so less oxygen can reach the foetus causing foetal hypoxia
HR increases by 8-10bpm and CO increases by about 40% in pregnancy, how does BP decrease in this time?
-peripheral vasodilation eg, E2 upregulates NO synthesis, which decreases TPR hugely
The low TPR in pregnancy allows more flow to uterus, placenta, muscles, kidney, skin..what change assists heat loss from skin?
Neoangiogensis
The lower TPR and SM relaxation mediated by progesterone has what effect on the GI tract?
Less motility which may cause constipation
Relaxed lower œsoph. Sphincter so acid reflux
How is acid reflux made worse by the large uterus combatted in pregnancy?
Small frequent meals
Folic acid does DNA production, growth, RBC production and more, from when to when should it be taken?
3 months before pregnancy
To week 12 of pregnancy
What effect does progesterone SM relaxation have on the urinary system?
- tract relaxes so more stasis (UTI risk)
- more flow through kidney glomerulus, more filtration so more frequent urination
- more clearance of creatinine, urea and Uric acid
CRH released from placenta into mother and foetal circulation can initiate labour. Through what process does this occur?
CRH—>ACTH—> more DHEA which increases prostoglandin availability in uteroplacental tissues to activate BFlow and cervical contractions
Prolactin increases through pregnancy, and suckling causes a surge in it. What prevents milk production in pregnancy?
-Progesterone
How does prolactin decrease chance of pregnancy for 3-6months of breastfeeding?
-inhibitory action on ovaries post-partum
At how many weeks can the fundus of the uterus be palpated above the pubic symphysis?
Week 12
Name 2 changes in the cervix during pregnancy?
- increased vascularity, becomes softer but still fibrous as high in collagen
- glands proliferate, lots of mucus forms a mucosal plug protecting vs infection
What happens to the cervix during labour?
-in labour, prostoglandins cause collagen/CT breakdown so cervix becomes soft and for baby to pass
Foetus uses about 5g glucose/kg each day. How does this and amino acids reach the baby?
Across placenta via facilitated diffusion
What is the dominant hormone in the foetus in the 3rd trimester? How/why?
Insulin
as B cells of pancereas -> hyperplasia
so more insulin increases fat stores in baby
What is colostrum in the first 24hrs? What does it cause the baby to do?
- 1st milk (7ml), is insufficient to meet baby’s energy needs
- forces baby to access its own fat stores
At birth how is the brain different?
- can use ketones
- cerebral metabolic rate (CMR) is low despite brain having the highest proportion of resting expenditure
In 3rd trimester, high insulin causes fat stores to build up. How does the baby access these stores when born? Hormones? Cortisol…GH….and
- surge in Adrenaline during labour triggers catabolism
- as plasma glucose falls at birth, a glucagon surge occurs (opposing insulin)
What 2 processes do babys use a lot to utilise stores for energy?
- Gluconeogenesis
- Ketogenesis (“suckling ketogenesis”)
What happens in B oxidation which occurs in the mitochondria of hepatocytes?
Glycerol and the 2 terminal carbons are removed from fats sequentially. Binds to Coenzyme A making lots of acetyl coA which is metabolised to ketone bodies.
Name 2 ketone bodies
Beta hydroxybuterate
Acetone
After a breast feed in the post prandial state, what happens in terms of hormones/storage?
-insulin allows storage in muscles and adipose
-in liver, excess glucose is converted to gycogen/fat
Active tissues e.g. brain take glucose direct from circulation
What are the rough components of breast milk?
50% fat
40% carbs (mostly lactose and some lipase)
What 4 problems may arise with baby’s metabolism of fuel?
- if demand is > supply
- hyperinsulinism
- counter-reg. hormone deficiency
- inborn errors in metabolism
Name 3 issues v small preterm babies have with metabolism?
- high metabolic demand but small stores
- immature metabolism (enzyme pathways)
- GI tract nor yet functionable so cant be fed
v small preterm babies and minerals e.g. calcium, phosphate issue?
-struggle to get minerals due to constraints in giving them IV and poor conc in breast milk and poor fat absorption so end up with metabolic bone disease.
IUGR is pathalogical what is the issue with metabolism balance?
- high demand esp. brain but stores in liver, muscle and fat are low
- immature gluconeogenic pathways
Hyperinsulinaemia often occurs when a baby’s mother is diabetic. Baby is often macrosomic. Why are they often hypoglycaemic babies?
- due to high exposure of maternal glucose it developed foetal hyperinsulinaemia and insulin is still high at birth
- at birth sudden withdrawal of glucose
What are 3 features of the overgrowth disorder “Beckwith Wiedemann”?
- macroglossia,
- midline abdo wall defects (e.g. exomphalmos, hernia)
- ear creases/pits
- hypoglycaemia
Name one group of rare syndromes that cause hyperinsulinaemia?
-islet cell dysregulation syndromes e.g. nesiodioblastosis
How may a CAH baby present? (CAH often is due to a 21OH deficiency so excess testosterone and lack of aldosterone)
-hypoglycaemia due to lack of cortisol as this is required for gluconeogenesis and to release glucose when fasting
Name 3 inborn errors in metabolism that cause neonatal hypoglycaemia
- Glycogen Storage Disease (type 1)
- Galactosaemia
- MCAD (medium chain acyl-coA dehydrogenase deficiency)
A deficiency in which enzyme causes -Glycogen Storage Disease (type 1)? Presentation?
- glucose 6 phosphatase deficiency. (it converts G6P to glucose)
- hypoglycaemia during stress/fasting
- newborn has lactic acidosis
- older child will have hepatomegaly
Which enzyme is missing in Galactosaemia? Its function?
Galactose-1-Phosphate Uridyl Transferase (Gal-1-Put)
In milk lactose is broken into glucose and galactose, then this enzyme breaks galactose to glucose.
Hence here toxic levels of Galactose-1-Phos. builds up
name 5 features of how galactosaemia may present?
- hypogycaemia
- jaundice
- liver disease
- poor feeding
- cataracts
- e coli sepsis
What is MCAD? medium chain acyl-coA dehydrogenase deficiency
- a genetic disorder of mitochondrial fatty acid beta-oxidation. (Autosomal Recessive)
- so fats in the body cant efficiently be broken down and used for energy.
name 3 features of how MCAD may present?
- Metabolic crisis due to hypoglycemia after fasting/stress..
- Weakness, vomiting, and seizures.
- Rarely, coma or sudden death
Name 5 minor common symptoms experienced in pregnancy e.g. tiredness..N&V..
- constipation
- heartburn/reflux
- mastalgia
- piles
- frequent urination
- backpain, headache, heat intolerance
How common are the following in the first trimester:
- Misscarriage
- Ectopic preg.
- Hyperemesis Gravidarium (constant vomiting)
- Misscarriage = 15%
- Ectopic preg. = 0.5-2%
- Hyperemesis Gravidarium = 2-5%
Suggest 4 maternal complications in the 2nd and 3rd trimester that can arise:
- UTI
- Anaemia
- Pre-eclampsia
- Gest. Diabetes
- Antepartum haemorrage
Suggest 3 foetal complications in the 2nd and 3rd trimester that can arise?
- Premature labour <37wks
- IUGR (weight under 5th percentile/2500g)
- Macrosomia (weight over 95th percentile/4500g)
One poss explanation for more UTI is increased diagnosis via the frequent appointments and urine samples. What 2 things in pregnancy physiologically increases chance of UTI?
- high progesterone –> SM v.dilation leading to urinary stasis so more infection
- immune suppression in pregnancy to prevent rejection of fetus –> more infection
Normal Hb 115-165g/L
Preg. Normal Hb 110-130g/L
(if less give what is deficient (Fe, B12, folate..)
Explain why normal Hb is less in pregnancy?
- despite more RBCs the increased body water (4.5 to 6L) causes haemodilution
- Max dilution occurs 28-30wks pregnant
Hb <100g/L in pregnancy should be investigated. Its often due to a deficiency e.g. of Fe, B12, folate..easily corrected. What other condition could be the cause?
-sickle cell, thalassaemia, blood dyscrasias e.g. leukaemia
If Hb<110g/L due to iron deficiency give ferrous sulfate, what if Hb<70g/L
Transfuse Hb/blood
What is gestational diabetes? Risks associated?
- After week 20 (not-pre-existing)
- more perinatal morbidity and mortality
- more maternal mobidity and mortality
Suggest 3 groups of women who are at increased risk of developing gestational diabetes:
- obese, -older
- family history of DM/-previous gestational DM
- PCOS
- previous baby >4.5kg
High risk gest. diabetes groups are screened at booking, all pregnancies are scanned at 28wks using what test?
OGTT
What are the risks of pre-existing diabetes and pregancy? What should be done preventatively?
- more risk of congenital malformation
- hypergly. at conception can be toxic to fetus (sacral agenesis….)
- need pre-pregnancy counselling 6months before to control sugar levels
Maternal hyper Glycaemia –> Foetal hyper Gly across placenta
-> foetal glycosuria which causes what? risk?
- Polyhydramnios
risks: malpresentation, cord prolapse, PPH (post partum haem.)
Maternal hyper Glycaemia –> Foetal hyper Gly across placenta
-> foetal hyperinsulinaemia and B cell hyperplasia
which causes what 3 complications? risk?
- Polycyntheamia (->jaundice)
- Neonatal hypoglyceamia
- Inhibition Surfactant (RDS)
- Macrosomia (long labour, APH)
How does hyperglycaemia lead to jaundice???
- placenta function is impaired so baby is born a bit hypoxic
- responds by making lots of RBCs (polycynth.)
- upon birth, excessive RBC breakdown -> jaundice
Management of a diabetic mother..aim is normoglycaemia..what/who is involved?
- diet, metformin, insulin
- obstetrician and diebetesologist
- US to detect congenital abnormalities, growth and polyhydramnios
- deliver at 38-40wks
What is the definition of PET (pre eclampsia)
A significant rise in BP (+30/+20 or HT) after 20wks on TWO separate occasions at least 2hrs apart and significant PROTEINURIA
In normal pregnancy how does BP decrease accommodating large placental flow despite 40% CO rise (more plasma vol).
BP=CO x TPR
TPR massively drops as progesterone causes vasodilation so overall BP drops
What happens in PET physiologically?..TPR? Placenta?
- vasodilation fails so TPR increases due to systematic vasocontriction/vasospasm
- faliure of 2nd wave of trophoblastic invasion at week 15-16 (placental disorder)
PET = yucky little vessel disease. What abnormalities in the vessels occur and may arise in microthrombosis?
- increased cap. permeability, fluid moves to interstitial space
- microangiopathy and endo. cell wall activation of platelets/coag. factors..can–> end organ infarction
What 3 theories offer an explanation to the poorly understood PET aeitiology:
Immuno
Vaso
Deficiency
- abnormal maternal immune reaction to trophoblast
- v.spastic substances e.g. NO, TNF, free radicals, altered RAAS sensitivity
- selenium, vit C / anti-oxidant deficiency
PET in mother can cause cerebral circulation bleeds, nephron damage and liver damage. What can the leaky vessels and proteinuria lead to ?
- fluid in brain/lungs
- less albumin in blood, lower oncotic p. more fluid loss
The foetus in PET is underperfused so sends blood to vital organs. How does the foetus/baby present?
Skinny (used all glycogen stores)
Unsymetrical IUGR
Less renal flow/less wee/oligohydramnios
What is a placental abnormality that can result in death that may occur in PET?
Placental abruption (separates from uterus wall)
When should a PET pregnancy deliver? Management?
- deliver at 37wks
- at 27wks Dr tries to prolong pregnancy with anti BP meds to stave off symptoms
- PET is progressive, will get worse until delivery
LABOUR is the process of uterine contractions and cervical dilation that enables the uterus to deliver…
the viable foetus (24wk+)
placenta and membranes
Stage 1 of labour is from onset of regular painful uterine contractions to full cervical dilation (10cm) what is stage 2 and 3
Stage 2-from 10cm to foetal delivery (0.5-1hr)
Stage 3-from this to delivery of placenta/membranes (riskiest)
1st stage of labour is made up of the latent phase then the active phase, what is the latent phase?
Latent: duration for cervix to become effaced and dilate 4cm, prostoglandins make it squishy + reg. contractions. approx 6hrs.
1st stage of labour is made up of the latent phase then the active phase, what is the active phase?
Active: cervix to dilate to 10cm, approx 1cm/hr. + strong uterine contractions (oxytocin)
What is a partogram (labour)
A partogram is a graphic representation of labour (rate of dilatation, descent of head, contraction frequency, vital signs..)
What is the alert line and action line used for in a labour partogram?
Alert is drawn 1cm/hr from start of active phase
Action is parrallel but 2cm to right
- women should be to the right of the alert line
- if they are to the right of the action line it means the labour is too slow and needs intervention to be sped up
What is the commonest cause of slow labour and how is it corrected? Any other causes?
Weal/uncoordinated contractions (esp. nulliparous)
Give oxytocin
-pelvis shape, fibroids, full bladder/rectum, big baby
Admission in labour. What is it important to adhere to?
The previously agreed action plan.
What are the 3 most important parts of managing labour stage 1?
- Reassurrance (1 to 1 support)
- Hydration and Ambulation
- Adequate pain reflief
Before giving oxytocin to a slow/complicated labour, what intervention should be attempted?
Artificially rupture the membranes to allow baby’s head to descend
2nd stage of labour is associated with what physiological changes..name 4
- vulval bleeding
- anal dilation
- urge to push
- increased resp rate
- unable to sit still
Slow labour is painful but also increases morbitity to both. What risks e.g. exhaustion -> dehydration cause slow labour to be dangerous?
- more intervention –> more infection risk
- operative delivery can –> foetal distress
- uterine rupture or vesicovaginal fistula
- post partum haemorrhage
To actively manage the 3rd stage of labour, what can be given when the anterior shoulder is delivered?
-intramuscular SYNTOMETRINE it is artificial oxytocin and ergometrin to stimulate short and prolonged contractions respectiv.
After the cord is clamped (+stops syntometrine going to baby) what does the midwife do to assist delivery of the rest?
- Hand above pubic symphysis, feel ant. uterus while controlled cord traction (pull) to check its not tugged down
- placenta pulled out, midwife checks it and membranes for completeness
Suggest 4 complications of the 3rd stage of pregnancy:
- placenta retained in uterus
- post partum haem.
- perineal trauma (2nd/3rd tear)
- perineal/pelvic haematoma
- uterine inversion
