Pregnancy + Birth + Pregnancy Loss Flashcards
+ fetal growth restriction
1
Q
Give an overview of an average human pregnancy
A
- last 40 weeks (9 months)
- made up of three trimesters
- 1st: <12 weeks
- 2nd: 12 - 26 weeks
- 3rd: 27 weeks- birth
2
Q
What are the things that change that the women body needs to change to accommodate for growing a child?
A
- supplying the baby with enough nutrients
- managing increased waste production: CO2, nitrogen compounds
- change in hormones to support pregnancy and prepare for delivery
- anatomical changes to accommodate the growing fetus ad preparing for labour
- the stress of delivery and potential haemorrhage
- postnatal recovery and breastfeeding require physiological changes
3
Q
What endocrine changes are seen in pregnancy?
- what do these hormones do?
A
-
BHCG: dramatic rise in the first days-weeks - released from the corpus luteum then by the placenta
- prevents corpus luteum involution,
- may stimulate the maternal thyroid
-
Progesterone: maintains myometrial quiescence
- inhibits other smooth muscles of the body GI and Urinary Tract
- stimulates the appetite, fat storage and the resp. centre
-
Oestrogen: breast growth, areolar enlargement
- promote uterine blood flow and myometrial growth
- promote cervical softening and expression of myometrial receptors at term
4
Q
How does the placenta act as an endocrine organ?
- hormones released
A
- It releases the following hormones
- hCG (human chorionic gonadotrophin) – produced by trophoblast, first detectable 8-9 days, peaks 8-9 weeks.
-
hPL (human placental lactogen) - Similar structure to prolactin and growth hormone.
- a larger placenta produces more hPL.
- Alters maternal carbohydrate and lipid metabolism to provide steady-state of glucose for fetal requirements
-
hPG (human placental gonadotrophin)- induces maternal insulin resistance to regulate fetal growth
- this may become a pathological process seen as GDM
-
CRH (corticotropin-releasing hormone)- implicated in human labour
- acts to increase prostaglandin synthesis
- may also directly stimulate myometrial contractility
- Progesterone
- Oestrogen
5
Q
What is the role of hPL - human placental lactogen?
A
- Similar structure to prolactin and growth hormone.
- a larger placenta produces more hPL.
- Alters maternal carbohydrate and lipid metabolism to provide steady-state of glucose for fetal requirements
- antagonises the effect of insulin and promotes lipolysis
- reduces glucose utilization and enhances amino acid transfer across the placenta
6
Q
What is the role of hPG - human placental gonadotropin?
A
- released by interstitial trophoblastic cells
- induces maternal insulin resistance to regulate fetal growth
- this may become a pathological process seen as GDM
7
Q
What is the role of hCG-human chorionic gonadotropin
A
- maintains corpus luteum secretion of prog & oest, decreases as the placental production of progesterone increases
- beta unit forms the basis of pregnancy testing.
- Alpha unit can mimic LH, FSH, and TSH
- Large quantities are released in molar pregnancy and multiple pregnancies
- High levels cause vomiting (hyperemesis)
8
Q
What is the role of Progesterone?
A
- Relaxes smooth muscle – everywhere!
- Maintains uterine quiescence by decreasing uterine electrical activity
- causes Constipation, gastric reflux, supra-pubic dysfunction
- acts as an Immune suppressor ( HLA )
- causes Lobulo-alveolar development in breasts
- Substrate for fetal adrenal corticoid synthesis eg cortisol
9
Q
What is the role of oestrogen?
A
- Growth of the uterus, cervical changes
- Development of ductal system of breasts
- Stimulation of prolactin synthesis
10
Q
What changes are seen in the Haematological System?
A
- 40% increase in plasma volume - 2.5L to 3.7L (8-10kg fluid weight gain)
-
25% increase in RBC
- these two factors leads to dilutional anaemia (peak at 32 weeks, exaggerated in multiple pregnancies)
- Plasma colloid osmotic pressure falls – shift of fluid into the extracellular space
-
Increase clotting factors –> hypercoagulable state
- Evolutionary balance between thrombosis and haemorrhage
- Increase plasma fibrinogen (increased ESR), platelets, factor VIII & von willebrand factor
11
Q
What changes are seen in the Cardiovascular system?
A
- Increased cardiac output
- occurs early on in pregnancy and plateaus at 24-30 weeks of gestation
- Decreased peripheral resistance
- Blood pressure
- proportional to change in CO and PR
- as peripheral resistance is often greater than CO, blood pressure may decrease at various stages of pregnancy
12
Q
How is peripheral vascular resistance impacted bu pregnancy?
A
- Peripheral vasodilatation (effect of progesterone)
- Peripheral resistance decreases by 35%
- Combined with increased cardiac output, results in slightly lower BP
- Decreased vascular resistance leads to lower blood pressure
13
Q
What changes are seen in the Respiratory system in Pregnancy?
A
- ventilation increased by 40% in first trimester
- tidal volume is increased to meet oxygen demands (deeper breathing rather than faster breathing)
- all done to meet increased O2 consumption
- increased inspiratory and expiratory reserve
- increased vital capacity
- decreased residual volume and total lung volume
- increased abdominal mass
- increased hyperventilation –> decreased PCO2 –> decreased HCO in-order maintain pH
- effects caused by progesterone and prostaglandin
*
14
Q
What is the clinical impact of the physiological changes on women?
A
- Splinting of diaphrgm, increased ventilation – sensation of increasing SOB
- Raised HR leads to palpitations
- Lots of cross over with symptoms for PE and known hypercoagulable state… leads to lots of investigations…!
- Excess plasma volume shifts causing oedema – peripheral
- Decreased exercise tolerance
- Low BP causing fainting / dizziness
15
Q
What are the dermatological and Musculoskeletal impacts of pregnancy?
A
- Increased lumbar lordosis
- Ligamentous laxity – pelvic girdle pain / pubis dysfunction
- Stretch marks
- Changes in skin pigmentation - Linea Nigra, melasma,
- darkened nipples
- Carpal Tunnel
- Sciatica
- Cramps
16
Q
What urological changes are seen in pregnancy?
A
- Kidney increases 1cm in size during normal pregnancy
- increased renal flow by 50%
- increased GFR (BUT tubular reabsorption capacity is unchanged) - decreased glucose reabsorption - glycosuria is common
- Plasma levels of creatinine and urea decrease in pregnancy
- Dilated ureters (progesterone)
- Increased pressure (increased urine frequency)
17
Q
What changes to Thyroid function are seen in pregnancy?
A
- Increased serum T3 and T4 levels
- increase in thyroid-binding globulin (caused by oestrogen
- levels of free T3 or T4 remain the same/ slightly fall as most are found in the bound form
18
Q
How is Labour initiated?
A
- maternal anterior pituitary is stimulated by factors from the fetal hypothalamus
- fetal hypothalamus-pituitary axis releases cortisol–> plays a role in cervical ripening
- stimulates inhibition of pre-pregnancy hormones
- progesterone
- stimulates an increase in pro-labour hormones
- oxytocin
- the Decidua of the placenta release prostaglandins
- this stimulates cervical ripening and stimulates uterine contractility
- this is through a direct effect and by upregulation of oxytocin
- there is also an inflammatory response that is thought to contribute to cervical ripening
19
Q
What is the effect of the initiation of labour?
A
- uterine contractions are stimulated
- there is mechanical stimulation of the uterus and cervix caused by stretching and stretching from the babies head causes the cervix to shorten and dilate?
20
Q
What are the stages of Labour?
A
- Latent phase
- 1st stage - 3rd stage of labour
21
Q
Explain the latent stage of labour
A
- long exhausting stage of labour, usually a sleepless period for women
- The cervix softens and shortens in response to prostaglandin
- Contractions caused by oxytocin and prostaglandin
- vary in intensity and refularity
22
Q
What are the stages of cervical effacement?
A
- measured in percentages
- when the cervix is completely effaced the cervical os starts to dilate
23
Q
How is Active labour Diagnosed?
A
- Painful regular contractions
- usually 3 every 10 minutes lasts 50-60seconds from beginning to end
- necessary power in order to give birth
- cervical effacement
- dilatation of the cervix of 4cms or more (digital examination)
- blood-stained mucous discharge, and spontaneous membrane rupture can also form part of the diagnosis
24
Q
Explain the First stage of Active Labour
A
- first stage is considered from the time, regular uterine activity associated with progressive effacement and dilatation of the cervix (active labour) until the cervix becomes fully dilated at 10cm
- progression of dilation is usually around 0.5cm/hour
- vaginal examination every 4 hours to check the progress
- can be faster if the mother is multiparous
25
How is the descent of the fetal head measured?
* progress is measured by the cervical dilation
* and the descent of the fetal head in relation to the pelvic brim and the ischial spines
26
Explain the Second stage of labour
* begins when the cervix is fully dilated and ends at the delivery of the baby
* the length can vary between nulliparous and parous women
* the length in nulliparous can be within 3 hrs of the start of the second stage or within 2 for parous women
* Progress is measured in by the descent and rotation of the fetal head on the examination and is in two distinct phases
* **Propulsive/passive phase**
* ****full dilatation until the head reaches the pelvic floor
* _the position of the head is usually occiputotransverse_
* there is no urge push
* **Expulsive/active phase**
* ****the head becomes visible and there is a strong involuntary desire to push
* delivery is usually in OA position
27
How does the fetus and the maternal pelvis work together to reach birth?
* a baby is born via the mechanism of _descent, flexion, rotation_ and _extension_
* approaches pelvis facing either the mothers left or right pelvis as this is the widest point
* as the baby descends further into the baby's head flexes it's chin into the chest and rotates it's head into the anterior-posterior diameter
* the coccyx is deflected backwards this is the space available during birth
28
Review the fetal skull and how this relates to delivery
* the **biparietal diameter** is the widest part of the skull
* the separate bones of the skull mould together during the mechanics of birth
* in normal birth, the **occiput** (back of the skull) presents anteriorly at the outlet of the pelvis
* the head flexes to present the smallest diameter to accommodate the limited space this is the:
* **_suboccipitobregmatic diameter_**
* **__**diameter from the back of the skull to the **anterior fontanelle (bregma)**
29
How is the head position assessed during birth?
- how would the structures be identified?
* the anterior and posterior fontanelle can be digitally assessed in a vaginal examination
* Anterior fontanelle (bregma)
* larger, diamond-shaped at the intersection of 4 sutures
* measures 2x3 cms
* this closes at 18 months
* Posterior fontanelle
* y-shaped at the intersection of 3 sutures
* closes at 6-8 weeks
30
What are the different presentations of the fetal skull at the pelvis?
- how would this affect birthing?
* Suboccipitobregmatic (9.5cms) = OA position
* Occitopitofrontal ( 11cms) = OP position
* Supraoccipitomental ( 13.5 cms) = brow
* Submentalbregmatic (9.5cms) = face
- the pelvic outlet is approx. 12,5cm in diameter: therefore a brow position would not be possible to deliver vaginally
31
Summaries the mechanism of birth
* Head at pelvic brim Occipital transverse (OT) position
* Flexion of neck (Suboccipitobregmatic)
* Head descends and engages
* Head reaches pelvic floor- rotates to Occipital Anterior
* Head delivers by extension
* Head “restitutes” (rotates to come in line with the shoulders)
* Shoulders rotate into anterior/posterior diameter of the pelvis (the widest part)
* Anterior shoulder delivered by lateral flexion from downward pressure on baby’s head
* Posterior shoulder by upward lateral flexion
32
Explain the Third stage of Labour
* this is the delivery of the placenta and membranes
* Chorion membrane
* Amnion membrane
* a blood loss of 300-500 mls is normal/ expected
* This delivery can be carried out via
* **Active management**
* oxytocin is given i.m into the maternal thigh
* control pull of the umbilical cord
* aids delivery of placenta and contraction of the placental bed
* decreases the risk of Postpartum haemorrhage (PPH)
* **Physiologically**
* a mother naturally expels the placenta and membranes with contractions
33
What fetal monitoring is done during labour?
* fetal monitoring is done to detect fetal hypoxia
* FBS (fetal blood sampling)
* small papillary stab on the scalp
* fetal heart rate can be measured by
* Intermittent auscultation by Pinard (ear trumpet) or Sonicaid
* every 15 minutes before and after a contraction in the first stage
* every 5 minutes in the second stage
* CTG (cardiotocograph) (can be used if any abnormalities are heard during auscultation)
* abdominal transducer can be used **or** a fetal scalp clip (FSE)
34
What is FBS, and when would it be contraindicated?
* A Fetal Blood Sample
* used to monitor pH and bass excess to check for hypoxia
* infection such as HIV and Hep B
* Fetal Bleeding Disorder
* Prematurity less than 32 weeks
35
What influences the incidence of twin pregnancies?
* increased maternal rate
* ethnicity
* increasing parity
* family history
* fertility treatment
36
How are multiple pregnancies defined?
* **Zygosity**
* ****refers to whether the twins have developed from a single ovum or from different ova
* dizygotic pregnancies have separate placentae
* **Chorionicity**
* ****this refers to the number of placentae
* **Amnionicity**
* ****refers to the number of amnionic sacs
37
Explain the different types of chorionicity that would form from various stages of embryo development
- 0-4 days
- 4-8 days
- 8- 14 days
\> 14days
* 0-4 days
* Dichorionic diamniotic (joined placentae)
* 4-8 days
* Monochorionic diamniotic
* 8- 14 days
* monochorionic monoamniotic
* \> 14days
* conjoined twins
38
Briefly explain Dichorionic twin pregnancies
* All dizygous twins are dichorionic
* Dichorionic twins must be diamniotic
* **Dichorionic = separate circulations**
* 1:3 monozygous twins are dichorionic
39
Briefly explain Monochorionic twin pregnancies
* Monozygous twins may be monochorionic (2/3) or dichorionic
* MC have vascularly joined placentae
* twin to twin transfusion (net blood flow from one twin to another)
* MC twins 3x increased loss rate
* MC twins usually diamniotic
* there are more fetal malformations and more fetal growth restriction
40
How are twin pregnancies diagnosed?
* uterine size
* ultrasound
* also used to determine chorionicity of the fetuses
41
What are some complications of Mulitple pregnancies?
* "everything except post-dates"
* Symptoms of pregnancy
* hyperemesis (severe and prolonged vomiting)
* increased risk of pre-eclampsia
* Anaemia
* Hypertension
* Intrauterine growth restriction
* Pre-term labour
* Delivery problems
* Perinatal mortality
42
What is twin-to-twin transfusion syndrome?
- management?
* there is a net blood flow from one twin to another through arterial to venous anastomoses in the shared placenta
* circulation of recipient becomes hyperdynamic - risk of hight output cardiac failure and polyhydramnios
* donor develops oliguria (low urine output) and polyhydramnios
* occurs in 10-15% of monochorionic multiple pregnancies and accounts for 15% of perinatal mortality in twins
* manage by early delivery by caesarean
43
What is the management of twin pregnancies in the first trimester?
* Discuss screening for chromosomal anomalies
* Determine chorionicity
* Discuss fetal reduction if triplets or more
44
What is the management of twin pregnancies in the second trimester?
* Detection of fetal abnormality
* Serial scans for growth for all
* DC monthly from 24 weeks
* Serial scans for TTTS if MC twins
* 2 weekly 16-28 weeks then monthly
* Maternal complications
45
What is the management for twin pregnancies in the third trimester?
* Scanning as in 2nd trimester
* Monitor blood pressure
* serial scans for growth of all fetuses
* serial scans for TTs if MC twins
* Pre-term labour
* Delivery planning
46
# Define the below terminology used in pregnancy loss
- Threatened miscarriage
- Inevitable miscarriage
- Incomplete miscarriage
- Complete miscarriage
- Missed miscarriage
- Molar pregnancy
* **Threatened miscarriage** – symptoms of bleeding /pain but intra-uterine pregnancy still present
* **Inevitable miscarriage** – symptoms of bleeding /pain, cervical os is open
* **Incomplete miscarriage** – symptoms of bleeding, os open, some tissue remaining
* **Complete miscarriage** – no tissue remaining
* **Missed miscarriage** (early fetal demise/ anembryonic pregnancy) – diagnosed at scan with no symptoms
* **Molar pregnancy** - fetus doesn't form properly in the womb and abnormal cells develop instead of a normal fetus. Known as ***hydatidiform mole***
* _******complete mole_, where there's a mass of abnormal cells in the womb and no foetus develops
* _partial mole_, where an abnormal fetus starts to form, but it can't survive or develop into a baby
47
What factors increase the risk of miscarriage?
* older Age mothers
* Obesity
* 25% increase risk with BMI \> 30 compared with normal BMI
* Antiphospholipid syndrome / SLE
* Parental chromosomal translocation
* Poorly controlled diabetes
* Alcohol, smoking, recreational drug use
* Uterine anomaly
* i.e. bicornuate nucleus
* (High levels of natural killer cells)
48
What are some typical presentations of miscarriage?
* Bleeding
* Pain
* Found at time of routine scan
* (i.e. missed miscarriage)
* (Loss of pregnancy symptoms)
* Acute collapse
* Cervical shock, hypotension, tachycardia, bleeding
* Sepsis
* Pyrexia, hypotension, tachycardia, raised resp rate, confusion
49
How is miscarriage managed?
* Conservative / expectant (40-80% success)
* Medical management – can be managed at home or on the ward dependent on size of pregnancy (CRL length) / patient preference
* Patients must be counselled re: expectations for bleeding and discomfort, potential risk of retained tissue
* Surgical management (SMM)
* Surgical risks include infection, bleeding, uterine perforation, cervical damage, retained tissue and need for a repeat procedure.
* Follow up - support/counselling,
50
What is recurrent miscarriage and how is this managed?
* 3 consecutive pregnancy losses \<24 weeks
* affects 1% of couples
* on third or later miscarriage offer karyotyping of the tissue
* chromosomal abnormalities affect 2-5% of couples
* attend miscarriage clinic
* Blood tests - thrombophilia screen, anti-cardiolipin antibodies, lupus anticoagulant
* **Antiphospholipid syndrome - 15%** of patients with recurrent miscarriage
* treatment (aspirin and LMWH) improves outcome
* check for Uterine anomalies: Ultrasound scan (3D scan) or hysteroscopy/laparoscopy
51
What are the risk factors for ectopic pregnancies?
* Previous ectopic pregnancy (15% risk after one)
* Tubal damage
* Previous tubal surgery
* History of pelvic infection / PID
* History of endometriosis
* History of subfertility/ IVF
* Presence of IUCD
* Use of progesterone-only contraception
* Cystic fibrosis
52
What are the 'Classic' Clinical presentations of an ectopic pregnancy?
- management
* Pain and bleeding 6-8 weeks gestation
* Positive pregnancy test
* Empty uterus on TV ultrasound scan
* Given options for conservative/expectant, medical (methotrexate), or surgical management
53
What is the 'modern' presentation of an ectopic pregnancy?
- management?
* Seen with EPAU minor symptoms in early pregnancy
* May be monitored over 48 hours to confirm diagnosis (using scans and hcg levels)
* Expectant management / medical / elective surgical
54
What would the hCG monitoring of a suspected ectopic or pregnancy of unknown location show?
* a normal intrauterine pregnancy would b expected to double in concentration every 48 hours
* in pregnancy of unknown location (not visible on the USS) a sub-optimal rise in hCG should provoke strong suspicion of an ectopic
55
What are the types of second trimester miscarriage?
- when is this considered a second trimester
* loss of a baby between 12-24 weeks
* Intra-uterine death or
* Premature labour/delivery
56
What are causes of intrauterine death?
* Fetal abnormality - structural/ chromosomal
* Infection
* Placental dysfunction, growth restriction
* SLE/ anti-phospholipid syndrome
57
What are causes of very Pre-term Labour?
* **Cervical weakness /incompetence**
* (e.g. due to multiple LLETZ- used to remove abnormal cell changes in the cervix)
* **Uterine abnormality**
* anomaly vs. acquired
* **Infection**
* inflammatory response causing uterine irritability and contractions
* **Rupture of membranes**
* can be a result of infection
* **Bleeding**
* e.g. from placenta = abruption (emergency)
58
When would cervical sutures be indicated?
_Indicated when_
* Past history of mid-trimester pregnancy loss
* Past history of cervical surgery
* Known uterine anomaly
* Cervical dilatation noted - on speculum examination or TV scan
* Usually inserted after 12 weeks gestation
* can be later in an emergency
* Can be inserted pre-pregnancy
* Transvaginal (most) or transabdominal
* risk of infection
59
What is considered a stillbirth?
* Baby delivered with no signs of life after 24 completed weeks of gestation
60
What are the causes of Stillbirth?
* Antepartum/ intrapartum bleeding
* Intrauterine growth restriction (eg. caused by maternal medical problems)
* Fetal abnormality- structural/ chromosomal
* Placental factors
* Infection
* Poorly controlled diabetes
61
What is Neonatal death?
* Early neonatal death: baby dies within 7 days of delivery
* Late neonatal death: baby dies within 7-28 completed days
62
What are causes of Neonatal death?
* Prematurity
* Congenital abnormalities
* Infection
* Intrapartum asphyxia
63
Why does diagnosing maternal hyperglycaemia matter?
* Morbidity in the offspring “from the uterus to the grave”
* prevents the exacerbation of the obesity & Type 2 diabetes epidemic
* Future Type 2 diabetes in the mother
64
What are the two types of Hyperglycaemia in pregnancy?
* Women with Normal Glucose tolerance
* Women with Abnormal Glucose tolerance
* Known Diabetes
* Unknown Diabetes or IGT
* there i
65
What are the possible scenarios that present hyperglycaemia during pregnancy?
* Pre-gestational Hyperglycaemia
* Type 1 Diabetes
* Type 2 Diabetes (known and unknown)
* Monogenic Diabetes
* Impaired Glucose Tolerance (IGT)
* “Gestational Diabetes” (GDM)
* Any newly found Abnormal GTT after the
* 1st trimester of pregnancy ( i.e. Diabetes or IGT )
66
What is Gestational Diabetes?
* Diabetes _or_ impaired glucose tolerance
* fasting glucose =/\> 5.6 mmol/l
* 2 hour GTT glucos =/\> 7.8mmo/l
* HAPO study shows that a 75g GTT with the following results would diagnose gestational diabetes based on the risk it presents to the fetus
* fasting 5.1 mmol/l
* 1 hour 10.0 mmol/l
* 2 hours 8.5 mmol/l
67
What changes are seen in maternal metabolism changes as the pregnancy progresses?
* Early pregnancy = **Facilitated Anabolism**
* Increased Insulin sensitivity
* Glucose concentration slightly lower
* Increased maternal energy stores
* Later Pregnancy = **Facilitated Catabolism**
* Increased Insulin resistance
* _Increased transplacental passage of nutrients_ leading to
* _Rapid fetal growth_
68
What is the effect of maternal hyperglycaemia in the 1st trimester?
* _Increased Fetal abnormalities_
* Fuel Mediated Teratogenesis
* Abnormal placental programming & development
* Increased risk of Pre-eclampsia
* Excessive glucose transport
69
What is the effect of MAternal Hyperglycaemia in the late 2nd and 3rd trimester?
* Excessive fat deposition
* and rapid growth in excess of what is desired
* adverse fetal programming
* epigenetic changes (increased methylation of certain genes)
70
What congenital malformations are due to maternal hyperglycemia?
* Neural tube defects
* Congenital cardiac abnormalities
* Sacral agenesis
* failure of the sacrum to develop - effects walking later on
* Renal problems
- high dose folic acid (5mg daily) to reduce this
71
What interventions can be done in the 1st trimester to get good diabetic control?
* Prepregnancy counselling
* Lifestyle Modification
* Intensive glucose monitoring
* If not on Insulin commence Insulin
* Optimize Insulin Regimen
* Basal Bolus or Pump
* Freestyle Libre or continuous glucose monitoring
72
What are risk factors for Hyperglycaemia of pregnancy?
* Previous gestastional diabetes
* Obesity
* PCOS
* Family hx of T2DM
* High-risk racial groups
* Hispanic people
* ppl from an Asian background
73
What problems are seen in late 2nd and 3rd-trimester pregnancies in maternal hyperglycaemia?
* Macrosomia causing
* difficult birth
* shoulder dystocia (difficult to deliver shoulder)
* breathing problems
* jaundice
* *_hypoglycemia_*
* hypocalcemia
* polycythemia
74
What are the lifelong/ long term effects of Hyperglycaemia in pregnancy on the fetus?
* Obesity
* Insulin resistance
* Type 2 diabetes
* Dyslipidaemia
* Hypertension
* Vascular disease
* Adverse neurodevelopmental outcomes?
75
What are the blood glucose targets for women with maternal hyperglycemia?
* Fasting glucose \< 5.1 mmo/l
* 1 hour postprandial glucose \< 7 (7.8) mmol/l
* Fetal Abdominal girth \< 70th centile (based on caucasian individuals)
* Less in Asians
76
What drug treatment is given to achieve glucose control in pregnancy
* Prepregnancy /1st-trimester hyperglycaemia
* switch to a Basal bolus Insulin regimen, (far better control)
* “Gestational” diabetes - diagnosed later in pregnancy
* lifestyle changes can usually be effective if not the following medication is appropriate
* **_Metformin_**
* Basal Insulin
* Basal bolus Insulin
* Glibenclamide (ONLY IF NO ALTERNATIVE)
77
How is gestational diabetes managed postpartum?
* Encourage Breast Feeding
* reduce inulin administration by 25% as they are more sensitive
* Maintain good Glycaemic control
* To prevent excess glucose in milk
* Reduce maternal weight gain
* Advice on next pregnancy
* Contraception advice - present random pregnancy
* Encourage long term glycemic control
78
How are those with Specific gestational diabetes mellitus managed postpartum in the long term?
* Screen for diabetes at 12 weeks postpartum
* _HbA1c_ +/- Fasting glucose, ( or GTT )
* Review GAD ect. antibody status if done (if they are at risk with other risk factors i.e weight or family presentations of endocrine diseases)
* Lifestyle advice
* Advice re next pregnancy
* Optimize exercise & Nutrition
* Pre-pregnancy GTT
* Annual glucose screening
* 50% develop type 2 diabetes at 10 years
79
What is the role of the Synctiotrophoblast layer in the early embryo?
* formed from cytotrophoblast cells (CTB)
* Syncytiotrophoblast burrows into the myometrium of the uterus
* it invades the maternal spiral arteries and starting the formation of the primary/secondary and tertiary villi
* which begins the process of forming the placenta
* they are in direct contract with the maternal blood and act as a barrier between the fetal and maternal blood (CTB cells also do this but they decrease as the pregnancy progresses)
* produce placental hormones
80
How is the placenta formed?
- what abnormality can arise from this?
* Syncytiotrophoblast invades decidua (endometrium)
* Cytotrophoblast cells erodes maternal spiral arteries and veins
* Spaces (**_lacunae_**) between the fill up with maternal blood
* very big spaces to allow lots of blood flow
* Followed by mesoderm that develops into fetal vessels
* Aiding the transfer of nutrients, O2, across a simple cellular barrier
* if the syncytiotrophoblast cells don't invade deeply enough into the maternal myometrium there is a narrow lacunae
* leads to reduced blood flow causing **pre-eclampsia**
81
How does the placenta act as an endocrine organ?
* Human chorionic gonadotrophin (HCG)
* maintenance of corpus luteum of pregnancy
* progesterone and oestrogen
* Human placental lactogen HPL
* growth, lactation
* carbohydrate and lipid
various others
82
What is transferred across the placenta?
* Gases – oxygen and carbon dioxide by simple diffusion
* Water and electrolytes
* Steroid hormones
* Proteins poor – only by pinocytosis
* Transfer of maternal antibodies IgG -starts at 12 weeks – mainly after 34 weeks
* therefore lack of protection for premature infants
83
What is this an image of?
- explain its significance
* Vasa praevia
* when the fetal blood vessels run across the cervical os
* As the internal os dilates in labour the vessels are stretched and exposed and can rupture leading to massive fetal blood loss and death.
* Diagnosed on Ultrasound using colour dopplers
* Management: delivery by Caesarean Section when the fetus is above 34 weeks.
84
Where is the position of the placenta in the uterus?
- what clinical presentation can there be?
* mainly fundal in the uterus (at the top)
* on the anterior or posterior walls
* can be "low-lying" or _placenta praevia_
* this is when it is near the cervical os
* this can sometimes manage itself in the third trimester of pregnancy, stretching of the lower part of the uterus causes it to thin and "move away"
* this is checked in the 20 week scan
85
What is this an image of?
- what is the clinical significance?
* Placenta Praevia
can cause
* massive bleeding in pregnancy
* usually painless bleeding
* fetal death
* maternal death
86
What are the clinical complications during pregnancy assocaited with the placenta?
## Footnote
*- what is the main cause of this?*
* poor maternal-fetal mixing of blood
* lack of oxygen and nutrients to the fetus
* causes fetal growth restriction
* and pre-eclampsia (raised blood pressure)
- *failure of trophoblastic invasion into maternal circulation at 12 & 18 weeks*
87
What is Placenta Accreta?
- treatment and risk factors
* When the placenta is unable to separate at birth
* the uterus cannot contract down and causes massive bleeding
* this occurs when the placenta has invaded too deep into the myometrium
* Treatment: hysterectomy
* Risk factors: scar in the uterus
* maybe due to a previous c-section
* fibroid
* surgically managed abortion
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What is a placental abruption?
- management and risk factors
* seperation of the placenta during pregnancy
* massive bleeding in pregnancy (often concealed)
* extremely painful
* concealed as the uterus is filled with blood, not the vagina as in placenta praevia
* can cause fetal and maternal death
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How does the placenta present in multiple pregnancies?
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What is the difference between growth and development in pregnancy?
* Development mostly happens in the first 12 weeks of pregnancy - when organs are being formed
* Growth - is when the baby gets bigger
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What does it mean if a fetus is SGA?
* means they are Small-for Gestational-Age
* this is using their estimated fetal weight (EFW) or abdominal circumference (AC)
* they are below the 10th centile for fetal growth scans
* not all small babies are synonymous with fetal growth restriction
* may be constitutionally small baby (look at parents)
* normal-sized baby that is showing reduced growth
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What ultrasound measurements are down to monitor fetal growth?
* Abdominal circumference (AC)
* Head circumference (HC)
* Femur length (FL)
* Liquor volume (LV)
* additional Doppler tests
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What are the three main causes of SGA fetuses?
* (1) “Normal” baby ie. constitutionally small
* Based on maternal size & ethnicity
* (2) Non-placenta mediated growth restriction
* eg. structural or chromosomal problem, fetal, infection, inborn errors of metabolism
* (3) Placenta mediated growth restriction
* eg. PET, hypertension, autoimmune disease (lupus etc.), thrombophilias, renal disease, diabetes
* groups 1 and 2 would show symmetrical UGR, whilst group 3 would show asymmetrical IUGR (reduced abdominal circumference)
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What are the risk factors of IUGR?
* Maternal age \> 40yrs
* Nulliparity
* Low or high maternal BMI
* Diabetes / Renal disease / APLS
* Smoking (nicotine is a vasoconstrictor)
* Maternal SGA
* IVF
* Previous SGA infant
* Previous stillbirth
* PAPP-A \< 0.4 MoM at combined screening
* Hypertension/PET/recurrent APH this pregnancy
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What is the effect of fetal growth restriction
* Deficient placental invasion --\> Reduced placental reserve --\> Fetal need exceeds supply --\> IUGR
* Hypoxia
* Fetal vascular redistribution to try and compensate
* Oliguria
* Abnormal CTG (Cardiotocography fetal heart monitor)
* ultimately Fetal death after compensation fails
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How is fetal growth restriction diagnosed?
* Clinical measurement of uterine size: Symphysis - fundal height (SFH)
* should roughly match the number of weeks pregnant they are
* Ultrasound scan gives a more accurate measurement of growth
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What does this fetal growth chart show?
- what does it indicate?
* asymmetrical growth restriction as only the abdominal circumference is reduced
* indicates a type 3 SGA fetus
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What does this fetal growth chart show?
- what does it indicate?
* symmetrical growth restriction as
* the head circumference
* the biparietal diameter of the head and
* the abdominal circumference are all reduced
* indicates either type 1 or type 2 SGA fetus
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Why is fetal abdominal circumference a good indicator of fetal growth?
* it's where the fetal liver is and the liver stores glycogen
* if the fetus is struggling it won't be able to store glycogen therefore eh abdominal circumference will be smaller
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What are the consequences of hypoxia in the fetus?
* blood flow redirected to more important areas --\> brain
* blood flow redirected away from other less important areas
* Gut
* Kidneys
* low fluid levels may indicate IUGR
* Lungs
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What are ultrasound findings in a fetus with IUGR?
* small abdominal circumference (liver)
* decreased amniotic fluid (produced by the kidneys, however their function has been reduced)
* increased blood flow to the brain
* looking at eh middle cerebral arteries in the brain using the doppler test
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What are the clinical features of IUGR?
* SFH (symphysis-fundal height) smaller than expected
* Baby’s movements lessen to conserve energy
* Fetal heart rate changes as hypoxia develop (as seen on CTG)
* Fetal death
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What is the management of a FGR baby?
* Serial ultrasound evaluation of fetal growth, liquor volume and fetal doppler
* Timing delivery depends on
* Gestational age
* Doppler studies
* Other risk factors
* aim to maximize fetal maturity and growth but minimize the risks of perinatal mortality and morbidity
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Explain fetal dopplers
- why are they used
- what do they look at
* used to differentiate the different type of SGA
* helps guides the timing of interventions
* intensive monitoring, antenatal glucocorticoid, early delivery
* Looks at blood flow and resistance in
* **Umbilical artery**
* ****should have low resistance
* **Middle cerebral artery**
* ****are usually constricted - can dilate if the baby is struggling as they increase blood flow to the brain
* **Ductus venousus**
* if blood flow is normal monitoring can continue, otherwise abnormal blood flow cay indicate expedited delivery
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What does this doppler show?
- what does it indicate?
* normal blood flow in the middle cerebral artery in the brain
* the peak = systole of the heart and during diastole flow is negative
* this scan shows an appropriate pressure difference in systole and diastole
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What does this doppler show?
- what does it indicate?
* shows increased blood flow as there is maintained blood flow during both systole and diastole rather than a pressure difference
* indicates there is fetal growth restriction and that the baby is compensating
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What is Betamethasone/ dexamethasone?
- when are they used
- what are their actions in pregnancy
* Steroids are given to mother x2 24hrs apart, if the baby needs to be delivered early
* this will cross the placenta and stimulate the aveoli cells to produce surfactant gene
* Surfactant stops the collapse of the aveoli cells by coating the cells and reducing the surface tension
* Helps prevent Respiratory Distress Syndrome which leads to neonatal death in premature babies
* Produced from 24- 34 weeks and usually the baby will have enough by 34 weeks in preparation for a term delivery
* hence this will be lacking in premature babies
