Session 6 Flashcards
- Where is hCG is released from? When does it peak?
- What is the function of hCG (human chorionic gonadotrophin)
- What other two hormones is important in maintaining pregancing
- syncytiotrophoblasts 10 weeks gestation
- Mimics LH prevent degeneration of CL
- Oestrogen and especially progesterone
- When does the placenta develop?
- Early development there is focus on ensuring development of the?
- 2nd week
- Placenta & fetal membranes
- What is the fate of the embryonic spaces (3)
- • The yolk sac disappears
- The amniotic sac enlarges
- The chorionic sac is occupied by the expanding amniotic sac
- In early embryonic development, the establishment of the ? takes precedent, why?
- What trophoblastic layer develops into the placenta?
- By the end of the second week, the conceptus has fully implanted & a fibrin clot has formed at the implantation site. The embryo (the bilaminar disc) is surrounded by two cavities in the amniotic cavity and the definitive yolk sac; this is suspended in the chorionic cavity by the connecting stalk.
As the embryo develops what changes occur to these sacs & why
- placenta to ensure the adequate support for the pregnancy
- cytotrophoblast & syncytiotrophoblast
- The yolk sac disappears to form the primitive gut tube and the amniotic sac enlarges to surround the embryo. Soon, the chorionic sac is occupied completely by the expanding amniotic sac and a potential space forms between the amnion and chorionic membrane.
As a consequence, the placenta forms as a specialisation of the chorionic membrane.
What does implantation achieve? (3) state the diffrent villi and give a brief description of each.
Allows exchange
- anchor the placenta
- establish maternal blood flow within the placenta
During implantation the placenta forms a mass of villi. Explain what the different villi contain.
– primary villi: early finger-like projections of trophoblast
– secondary villi: invasion of mesenchyme into core
– tertiary villi: invasion of mesenchyme core by fetal vessels
(placental membrane progressively thins)
Implantation defects (4)
ashermans syndrome -> adhesions -> oligomenorrhea -> pain menstration
cervical stenosis -> oligomenorrhea
Fitz-hugh-Curtis -> due to PID -> RUQ pain -> perihepatic adhesions (liver and diaphragm) -> causes peritonitis
Implantation in the wrong place
– Ectopic pregnancy
– Placenta praevia
Incomplete invasion
– placental insufficiency
– pre-eclampsia
- What three things can cause shoulder pain
- What is an ectopic pregnancy? Symptoms
- What is placental praevia
- Gallstones, ectopic pregnancy, heart attack
- implantation at site other than uterine body (commonly Fallopian tube)
- can be peritoneal or ovarian
Symptoms;
- shoulder tip pian + iliac fossa pain
- uterine bleeding
3. - implantation in the lower uterine segment/ cervical opening - can cause haemorrhage in pregnancy
- can require C-section delivery
- bleeding in third trimester
- What controls invasion in implantation?
- How does invasion differ in ectopic pregnancies?
- What aspect is the image showing?
- endometrium -> decidua (presence of a conceptus)
- No decidua
- Fetal
- State the structure of the chorionic villus
- What will these villi be in contact with?
- Other than villi for exchange what other villi are present?
- From the tips of large anchoring cytotrophoblast cells spill out into the endometrium creating a shell and also contribute to the remodelling the walls of maternal spiral arterioles. Hence these cells are now technically outermost but are not involved in transport and/or exchange. The chorionic plate is the “base” of the placental disc (i.e. roots of the tree) and is composed of the trophoblastic part and the mesoderm part.
- One umbilical vein, two umbilical arteries
- maternal blood (uteroplacental circulation)
syncytiotrophoblastic
- Anchoring villi: cross the intervillous space and attach directly to the maternal uterine decidia (uterine lining (endometrium) during a pregnancy, which forms the maternal part of the placenta).
4.
- Who has spiral arteries?
- The mother
- Why are the arteries spiral?
- What do the arteries supply?
- Explain how the placenta changes?
- Low resistance vascular beds = high flow
- intervillous space
- Image
What is the umbilical cord composed of?
• Two umbilical arteries
– Deoxygenated blood from fetus to placenta
• One umbilical vein
– Oxygenated blood from placenta to fetus
Describe the role of the placenta as an endocrine organ supporting pregnancy LO
Hormones produced by the placenta are:
Human Chorionic Gonadotrophin (hCG)
- When is it produce during pregnancy?
- Why is it produced?
- What is it produced by?
- Clinical significance?
- first 2 months of pregnancy
- supports the secretory function of corpus luteum (continue production of progesterone & oestrogen?)
- Syncytiotrophoblast
- • excreted in maternal urine therefore used as the basis for pregnancy testing
• trophoblast disease
– molar pregnancy (hydatidiform mole)
– choriocarcinoma
Explain the factors influencing the passive diffusion of substances across the placenta LO
- Name the placental steroid hormones
What week does it start releasing hormones?
- Which placental hormones influence maternal metabolism? Explain how.
- Which molecules pass by simple diffusion?
- Facilitated diffusion
- progesterone & oestrogen,
placental production takes over from corpus luteum by the 11th week
-
Progesterone - increased appetite
* *hCS / hPL** - increases glucose availability to fetus - • water • electrolytes • urea & uric acid • gases
- glucose transport
Identify the major substances which are actively transported across the placenta LO
- Where are AT transporters expressed?
- What is actively transported?
- – amino acids
– iron
– vitamins
- syncytiotrophoblast
Explain the function of the placenta as a provider of passive maternal immunity to the neonate LO
receptor-mediated process/ endocytosis
IgG only (concentrations exceed those in maternal circulation)
State how gasses, urea, FFAs, glucose, aa & IgG transport across the membrane
Name 5 harmful substances that can pass the placenta
• thalidomide
– Limb defects (Destroyed small blood vessels in the developing limbs)
• Alcohol
– FAS and ARND (Can SS via diffusion Complete alcohol syndrome)
• therapeutic drugs
– Anti-epileptic drugs – Warfarin – ACE inhibitors
• drugs of abuse
– Dependency in the fetus and newborn
• smoking
What points of embryogenesis is the embryo susceptible?
• Pre-embryonic
– lethal effects
• Embryonic
– ++ sensitive
– narrow windows for some systems
• Fetal
– +/- sensitive
• After embryonic period, risk of structural defects very low
– Except CNS
Define direct & indirect maternal causes of death
Which one is a more common cause of death direct or indirect?
Indirect -> 75% of maternal deaths have a pre-existing medical condition
- Diabetes (prevent fetal deaths and macrosomn\ia )
- Cardiac disease
- Neurological conditions- epilepsy- rv meds
- Essential hypertension (BP tablets suitable for pregnancy - labetalol, nifedipine (SR)or methyl dopa (a2 agonist) Ace Inh and statins contraindicated
- Rheumatological conditions (ensure not on cytotoxic medication e.g. methotrexate)
- Respiratory disease- CF weight gain, use inhaler if asthmatic
- Previous spinal surgery (further imaging?)
- Bariatric surgery (avoid pregnancy for 12-18 months, GTT, 5mg folic acid, Vitamin D)
- HIV (Discuss starting HAART, mode of delivery, breast feeding contraindicated; antiretrovirals and postnatal testing in infant)
At around 8 - 12 weeks since conception pregnant women need to book an appointment. What must be checked?
Infections in pregnancy
Draw a diagram showing the physiological changes in pregnancy
What is preeclampsia
BP > 140/90
> 0.3 g/save protein in a 24 hour urine collection
> 20 weeks gestestation will present
Fibrosis of the uterine arteries (cannot dilate) -> intrauterine growth restriction/death
Reduced perfusion if the placenta -> inflammatory markers are released
Causes vasoconstriction due to endothelial dysfunction -> hypertension
Causes oedema -> cerebral (eclampsia), lung,
Causes vasospasm -> kidneys (oligouria, proteinuria), retina (blurry), liver RUQ pain (inc liver enzymes)
Damage to endothelial wall -> thrombi
How does our metabolism of glucose change during pregnancy?
There is a decrease in insulin sensitivity -> more glucose in the blood to feed the fetus
- How does gestational diabetes occur?
- Risk factors?
- Complications?
- Insulting resistance (image)
- GTT if BMI>30, family history of diabetes, PCOS, long term steroid use
- fetal macrosomia, stillbirth, neonatal hypoglyceamla
more glucose to fetus, pancreas produces more insulin, after laabour reduction in glucose, but still overactive pancreatic B-cells = hypoglycaemia
How do we manage the mother?
How do we manage the fetus?
Management of patients with pre eclampsia
State the high & low risk factors for pre eclampsia
Symptoms that occur before an eclamptic episode include:
Low dose aspirin from 12 weeks (can be started up to 20 wk) continue until delivery (75mg od)
severe headache
problems with vision, such as blurring or flashing before the eyes
severe pain just below the ribs
vomiting
sudden swelling of the face, hands or feet
State how the clotting factors change during pregnancy
More coaguable
State the risks for venous thromboembolism in pregnancy
- If 3 or more current or persisting risk factors consider AN prophylactic LMWH.
- If 2 or more persisting risk factors should be considered for LMWH for 7 days PN
BMI > 40kg/m2, LMWH for 7 days PN
Emergency caesarean section consider LMWH for 7 days PN
Post elective caesarean section who have one or more additional risk factors (eg BMI>35) consider LMWH for 7 days PN.
Women with VTE before the current pregnancy should be offered LMWH for 6 weeks following delivery.
In women who have additional persistent (lasting more than 7 days postpartum) risk factors, such as prolonged admission or wound infection, thromboprophylaxis should be extended for up to 6 weeks or until the additional risk factors are no longer present.
What is the effect of pregnancy on the CV, respiratory, urinary, metabolic & peripheral vascular system.
State what changes are seen in each trimester.
What changes are seen on an ECG of a pregnant woman
ECG changes that are physiological, not pathological, during pregnancy are:
- atrial and ventricular ectopics
- left shift in the QRS axis
- small Q wave and inverted T wave in lead III
- ST segment depression and T wave inversion in the inferior and lateral leads.
- ST ELEVATION IS NOT NORMAL IN PREGNANCY- think MI
If a patient is obese and pregnant how should we manage the patient
What are obese pregnant women at risk of?
- Miscarriage,
- Fetal congenital anomaly,
- Thromboembolism
- Gestational diabetes
- Pre-eclampsia,
- Dysfunctional labour,
- Shoulder dystocia
- Postpartum haemorrhage,
- Wound infections
- Stillbirth neonatal death
- Higher caesarean section rate
- Lower breastfeeding rate
State which commonly used drugs should be avoided during pregnancy
