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4/ RED > Placenta > Flashcards

Placenta Flashcards

1
Q

When is clinical gestation timed from?

A

1st day of last menstrual period

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2
Q

During what part of pregnancy does the placenta form?

A

From 3 weeks to 16 weeks.

Foetus is only dependent on placenta in the last trimester

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3
Q

What are the characteristics of the endometrium during the mid-luteal phase?

A
  • receptive
  • secretory activty peaks
  • endometrial cells rich in glycogen and lipids (14mm thick)
  • glands increase in number and size
  • maintained by high progesterone and oestrogen levels
  • endometrial receptivity is marked by changes on surface epithelium
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4
Q

What are pinopodes?

A

The structures found on the surface of the endometrium, only apparent during the implantation window
They cover the cilia underneath them, envelope embryo
Surface area for fluid absorption, help attract blastocyst

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5
Q

What is implantation? How does it occur? What are the 3 stages?

A
  • Embryo attachment and penetration of the endometrium and maternal circulatory system to form the placenta
  • Blastocyst enters the uterus bathed in the uterine secretions for 1-3 days proper to hatching from the zona pellucida
  • Apposition = blastocyst loosely associates with uterine wall
  • Attachment = firm adhesion
  • Invasion = blastocyst attachent to the uterine wall triggers enzyme production, degrades and invades the glycogen rich stroma, provides further nutrient support
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6
Q

Describe the process of decidualisation of the endometrium

A
  • induced by progesterone
  • oedema, changes in ECM, vascular remodelling/angiogenesis, leucocyte inflation (uNK cells)
  • endometrial stromal cells undergo morphological and biochemical changes from fibroblast like to polygonal
  • store glycogen and lipids
  • secrete decidual proteins e.g. prolactin, IGFBP-1, tissue factor, VEGF, PIGF, IL-15
  • The decidua completely surrounds the implanted blastocyst by day 10, most is shed at parturition
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7
Q

What factors influence implantation of the blastocyst?

A
  • ## oxygen tension, growth factors and cytokines, transcription factors, regulation of trophoblast proliferation and differentiation,
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8
Q

The trophectoderm gives rise to what three main types of trophobalast?

A
  1. cytotrophoblast (villous cytotrophoblasts)
  2. suncytiotrophoblast - forms by fusion of villous cytotrophoblasts
  3. extravillous trophoblasts (EVT) - interstitial, endovascular
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9
Q

What are the normal dimensions of the placenta at term?

A

15-25cm
2.5-3cm thick
500g

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10
Q

Describe the structures of the placenta

A
  • 2 x umbilical arteries
  • 1 x umbilical vein
  • chorionic plate
  • amniochorionic membrane
  • intervillous space
  • amnion and chorion
  • cotyledon
  • anchoring villus
  • cytotrophoblastic shell
  • spiral arteries, endometrial veins
  • myometrium
  • decidua
  • placental septum
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11
Q

What are the 3 main classifications of the placenta? These are based on the organisation and separation of fetal and maternal blood supplies

A
  1. Haemochoroidal - the chorion is in direct contact with the blood = HUMAN
  2. Endotheliochoroidal - the maternal blood vessel endothelium comes in direct contact with the chorion = DOG, CAT
  3. Epitheliochoroidal - the most primitive form - the maternal epithelium of the uterus comes into contact with the chorion = COWS, PIGS
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12
Q

Describe blastocyst nutrition

A
  • O2 and nutrients reach the developing ember by diffusion from the surrounding decidua = histiotrophic neutron)
  • The initial phases of development occur at low O2 tensions
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13
Q

List the steps of the development of placental villi

A
  1. Lacunae formation 6-10 days
  2. Primary villi 11-21 days
  3. Secondary villi 11-21 days
  4. Tertiary villi 11-21 days
  5. Intermediate/mature villi
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14
Q

Describe lacunae formation

A
  • lacunae form in the syncytiotrophoblast
  • syncytiotrophoblast invades and erode maternal capillaries
  • these anastomoses with trophoblast lacunae to form sinusoids
  • intervillous space develops
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15
Q

Describe the primary villi

A

Day 11-13

  • cytotrophoblasts invade
  • cytotrophoblast extend and invade into syncytiotrophoblast layer form finger like projections in the decidua
  • primary villi cancer the entire surface of the blastocysts - ‘hairy ball’
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16
Q

Describe the secondary villi

A
  • extraembryonic mesoderm (mesoblast) invade the core the of primary villous
  • mesoderm covers the entire surface of the chorionic sac
  • villi continue to extend into the decidua between the blood filled lacunae/sinusoids
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17
Q

Describe the tertiary villi

A
  • mesodermal cells differentiate to form endothelial cells and other cell types
  • blood vessels form anarterio-capillary network in the villi
  • these vessels fuse with developing vessels in the stalk - to link the fatal blood system via invading vessels from the umbilical cord
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18
Q

Describe the structure of mature placental villi, x3 types

A

Stem villi - basal part of villi attached to chorionic plate
Branch/intermediate villi - project from the sides of stem villi
Terminal villi - swellings at the tops of branch villi contain terminal vessels - form convoluted knots where the majority of exchange takes place - continue to be produced throughout gestation
- the cytotrophoblast layer becomes very thin, but remains mostly intact (80% coverage in full term placenta)

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19
Q

Describe spiral arteries and how and why they are transformed

A

Spiral arteries
- resistance easels supplying the endometrium/decidua
- coiled appearance in the inner myometrium and decidua
- 100-150 arteries are transformed
- diameter is increased 10-fold (200um –> 2mm)
Transformation
–> essenstial to establish a low resistance high flow blood supply to the intervillous space
- critical for normal pregnancy

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20
Q

Describe extravillous trophoblast outgrowth in the first trimester

A

Cytotrophoblasts at the end of the anchoring villi proliferate and differentiate to form EVT
Anchoring villi cross the intervillous space and attach to the maternal decidua
- cytotrophoblast columns form at the tops of anchoring villi
- extravillous trophoblasts (EVT) differentiate and form interstitial and endovascualr EVT
- EVT invade the decidua and occlude the spiral arteries
- replace the endothelium and smooth muscle cells forming the endovascualr trophoblast layer
- establish normal utero-placental dynamics

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21
Q

Describe the process of the remodelling the spiral arteries

A
  • EVT plus the spiral arteries - reduce blood flow to the developing placenta
  • Creates a low oxygen envirnonment —> protects foetus from oxidative stress
  • EVT plugs breakdown initiating blood flow to intervillous space >14 weeks
22
Q

What is the role of the maternal immune system in remodelling of the spiral arteries?

A
  • uterine natural killer cells (uNK cells) make up 70% of inflammatory cells in decidua
  • produce many cytokines and initiate/promote remodelling
23
Q

What are the four functions of the placenta?

A

transport
metabolism
endocrine
immune privilege

24
Q

What are the phases of nutritin in pregnancy and at what gestation does each occur?

A
  • histotrophic phase (week 8) = O2 20mmHg
    Placental perfusion intimated week 12-14
  • haematrophic phase (week 14) = O2 60mmHg
25
Q

What kind of a relationship is the transport relationship across the placenta described as?

A

Parabiotic relationship between mother foetus –> foetus is dependent on maternal provision of nutrition, O2, slats, organic precursors etc, and removal of waste products CO2, urea etx. across the placenta

26
Q

How are substances transported across the placenta?
What substances are not tranpsorted?
What substances are harmful?

A

Diffusion
- O2, CO2, Na+, urea, fatty acids, sugars, non-conjugated steroids, thyroxine,
Active Transport
- amino acids, iron, Ca2+
Not Transported
- conjugated steroids, nucleotides, most bacteria
Harmful
- cocaine, alcohol, caffeine, tetracycline etc.

27
Q

Describe the maternal adaptations to meet the increasing oxygen/nutrient demand of the growing foetus

A
  • uterine blood flow increases 20 fold during pregnancy via uterine (+ovarian) arteries
  • cardiac output increases by 30-40%
  • > 25% of CO goes to placenta
  • increased maternal blood volume 40%
  • increased ventilation rate
28
Q

Describe the pathway of foetal blood flow in the placenta

A

umbilical arteries –> foetal capillaries (within villi: stem intermediate terminal) –> umbilical vein

29
Q

Define haematrophic nutrition

A

beyond week 14 maternal blood delivers nutrients to the foetal circulation across the placenta

30
Q

What are the 4layers that separate the maternal and foetal circulations?

A
  • syncytiotrophoblast
  • cytotrophoblasts
  • connect tissue
  • foetal capillary endothelium
31
Q

How much blood is contained in the intervillous space of a mature placenta?
How much blood can be exchagend a minute?

A

150ml of blood

3-4ml per minute

32
Q

Describe gas exchange across the placenta

A
  • O2 and CO2 by passive diffusion
  • 40% more Hb in foetal blood vs adult
  • Foetal O2-Hb curve left shifted of adult
  • Higher affinity for O2, achieves saturation at lower PO2
  • Simulatenous movement of CO2 on a concentration gradient back to the mother
  • Double Bohr shift results in increased of pH on foetal side - promotes O2 uptake at lower PO2
33
Q

Describe glucose-carbohydrate transport and metabolism in the placenta

A
  • uptake by insulin sensitive hexose transporters (GLUT3, GLUT1)
  • maternal insulin regulates glucose - increases glycogen and adopts stores
  • maternal tissues show insulin insensitivity/resitsnce (due to human placental lactogen) promoting transfer of blood glucose to the placenta
  • glucose is also metabolised to lactate which is used as an energy source by the foetus
34
Q

Describe amino acids and urea transport and metabolism

A
  • foetus regulates maternal amino acid metabolism through progesterone
  • mother retains extra amino acids and transports them to foetal circulation
  • some are metabolised e.g. serine –> glycine
  • foetal urea diffuses passively into maternal blood
35
Q

Describe lipid transport across the placenta

A

extracellular lipases release fatty acids from maternal lipoproteins - intracellular binding proteins (FABPs) transport the fatty acids in the cytosol of the syncytiotrophoblast

36
Q

Describe water and electrolyte exchange in the placenta

A
  • exchange in water occurs in placental and non-placental chorion at the amnion - amniotic fluid increases from 15ml at 8wks to 250ml at 20 wks, net production decreases to 0 by 24wks
  • Na+ and other electrodes transfer readily across the placenta
37
Q

Describe iron transport

A
  • in foetal and maternal blood both free and bound to transferrin
  • enhanced absorption through gestation to vocoder losss to foetus, placenta and blood loss during labour
38
Q

Describe calcium transport

A
  • demand for foetal ossification in 3rd trimester

- Ca2+ absorption is enhanced and transferred to foetal circulation

39
Q

What vitamins need to be transported across the placenta?

A
  • folic acid

- vitamin B12

40
Q

What infectious agents can cross the placenta?

A 
Viruses 
- cytomegalovirus 
- rubella 
- coxsackle
- varicella
- poliio
- HIV
Bacteria 
- spirochetes e.g. syphilis, listeria, lymes disease 
Protozoa 
- toxoplasma
41
Q

How is passive immunity transferred and to what?

A 
IgG transferred by pinocytosis 
Provide passive post-natal immunity to:
- diphtheria 
- smallpox
- measles
- chickenpox 
- whooping cough
42
Q

Describe poor EVT invasion of the maternal spiral arteries and its consequences

A
  • migration of EVTs is under tight temporal-spatial control, disturbances in this process can result in significant loss of placental function
  • IUGR/early onset pre-eclampsia due to insuffiecnt penetration by EVTs - shallow invasion
  • premature loss of EVT plugs - early initiation of blood flow to placenta may lead to miscarriage
43
Q

Describe the different between transformation of the maternal spiral arteries in a normal pregnancy and in a growth restricted one

A

Normal
- Invasion of trophoblast into myometrium
- maternal arteries now wide and low resistance to flow
- aired by interivtial EVT, and giant cells
Growth restricted
- no deep invasion, invasion only into decidua
- leads too high pressure flow
- vasoconstriction –> pulsatile flow
- iscaemia reperfusion injury/oxidative stress
- damage to villi

44
Q

What is pre-eclampsia?

A
  • maternal system syndrome caused by abdnoral placentation in first trimers - clinical symptoms present from 20 weeks onwards
  • 3-5% of pregnancies in West
  • severe early onset PE - 0.5% of pregnancy
  • 30% of PE cases are associate with IUGR
  • only cure is delivery of the placenta
45
Q

What are the maternal symptoms of pre-eclampsia?

A
  • symptoms develop in 2nd/3rd trimester (>20 weeks)
  • hypertension (>140/90mmHg)
  • proteinuria - .300mg/l or 2+ dipstick
  • headache
  • HELLP sundrome in 20% of cases
  • DIC in 20% of HELLP cases
  • seizures - eclamspoa
  • early onset (<32 weeks) tends to be more severe
46
Q

What are the risk factors for pre-eclampsia?

A
  • 7 fold greater if previous PE pregnancy
  • maternal or paternal history of PE
  • increased inter-pregnancy interval
  • multiple gestation
  • maternal age >40 years
  • insulin resistance, diabetes, obesity, metabolic syndrome, vascular inflammation, pre-existing hypertension
47
Q

What is the underlying pathology of the placenta and the mother in pre-eclampsia?

A 
Placenta 
- abnormal trophoblast invasion
- reduced differentiation and transport 
- altered trophoblast secretion s
- enhanced trophoblast apoptosis 
- increased fibrin deposition 
Mother 
- systemic endothelial activation 
- systemic inflammatory response
48
Q

What is IUGR?
How does it come about?
What are its consequences?

A
  • occurs in 8-14% of normal pregnancies - associate dight pregnancy induced hupertensn - early onset PE
  • nod flow on both sides of the placenta compromised
  • O2 passes across by simple diffusion - reduced flow leads to foetal hypoxia
  • reduced fatty acid transfer
  • amino acid transport is compromised
  • reduced ion transport
  • acidosis
  • reduced bone mineralisation in 3rd trimester
49
Q

What is placenta previa? How does it come about? What are the different types?

A

Placenta previa occurs in 3-6 per 1000 pregnancies

  • blastocysts usually implant high on posterior wall of the uterus
  • increased risk of placental abruption
  • classified on the degree of coverage of the cervis/os
50
Q

What is placenta accreta?

A
  • results from excessive trophoblast invasion
  • placenta invades and is inseparable from uterine wall
  • indentified before parturition on US scan
  • can lead to vaginal bleeding in 3rd trimester
  • associated with cases of placenta praaevia
  • associated with myometiral scarring from previous C-sections
  • risk of maternal haemorrhage
  • pre-term C section/hysterectomy may be required

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