11. Fetal Period Flashcards
FETAL PERIOD starts with what process
PLACENTAL INVASION
important part of PLACENTATION
Establishing BLOOD SUPPLY
what is needed for establishing a BLOOD SUPPLY in PLACENTA formation
SPIRAL ARTERY REMODELING
Invasion of SYNCYTIOTROPHOBLASTS causes Small SPIRAL ARTERIES to
- have LARGE LUMEN
- Disrupts muscular layer so LOSE SENSITIVITY to VASOCONSTRICTORS
ALLOW MAXIMUM GAS EXCHANGE
in PLACENTAL DEVELOPMENT when are TERMINAL VILLI formed
by 20 WEEKS
HORMONE PRODUCTION by PLACENTA
- hCG (human chorionic gonadotrophin)
- hPL (human placental lactogen)
- PROGESTERONE
PLACENTA forms a …. BARRIER
IMMUNOLOGICAL BARRIER
- LYMPHOID CELLS
- PHAGOCYTES
when does FETAL SKIN become IMPERMEABLE to FLUID EXCHANGE
16 WEEKS
what is AMNIOTIC FLUID PRODUCED by
FETAL URINE,
swallowed and recycled by fetus
bathes fetal LUNGS
AMNIOTIC FLUID (measurable by ultrasound scan) increases to PEAK of … at how many weeks, before REDUCING to … by ..
800 ml at 30 WEEKS
reduces
approx 400 ml by 42 weeks
AMNIOTIC FLUID is PREDOMINANTLY..
WATER
characteristics of AMNIOTIC FLUID
PROTECTIVE
has HOMEOSTATIC EFFECTS
conditions that can cause INCREASED AMNIOTIC FLUID
- DIABETES
- MACROSOMIA (larger fetus than normal)
- FETAL PATHOLOGIES
conditions that can cause DECREASED AMNIOTIC FLUID
- IUGR (intrauterine growth restriction - not growing as expected)
- RENAL PATHOLOGIES (kidneys)
- RUPTURED MEMBRANES
things that happen with LIMBS during FETAL DEVELOPMENT
- NAILS form
- fingers SEPARATE
- BONES remain mostly CARTILAGINOUS and only HARDEN SLOWLY
- INCREASE in fetal MOVEMENTS from 25 weeks (although start movements earlier)
things that happen with FACE and HEAD during FETAL DEVELOPMENT
- ENLARGEMENT of the SKULL (sutures do not fuse until CHILDHOOD)
- EXTERNAL EARS form
- SUCKING REFELEXES observed from 17 WEEKS
- HAIR begins to grow from 20 WEEKS
- Face becomes more human-like
when do SUTURES of SKULL FUSE
ONLY in CHILDHOOD
- Do not fuse premature or can cause problems in brain development
when do SUCKING REFLEXES BEGIN
17 WEEKS
when does HAIR start to GROW
20 WEEKS
what happens in ABDOMINAL DEVELOPMENT
- ROTATION and HERNIATION of GUT (by 12 WEEKS)
- SWALLOWING develops
- DEPOSITION of BODY FAT (on fetus around abdomen)
- DIAPHRAGM CLOSES (separation between thorax and abdominal cavity)
in ABDOMINAL GROWTH
when does ROTATION and HERNIATION (protruding through /rupture) of the GUT take place
By WEEK 12
(allows space for gut to grow and rotate before returning to proper place IN abdomen)
when do KIDNEYS BEGIN to PRODUCE URINE
FROM 16 WEEKS
VOLUME of URINE EXCRETED by KIDNEYS (from 16 weeks) INCREASES to …. at 40 WEEKS
38 ml/hour at 40 WEEKS
when is RENAL DEVELOPMENT only COMPLETE
36 WEEKS
EXTERNAL GENITALIA visible from..
12 WEEKS
when do TESTICLES DESCEND (from pelvis into scrotum)
16 WEEKS
in FEMALE FETUS, when are the OOCYTES at their MAXIMUM number
20 WEEKS
what happens in BRAIN DEVELOPMENT
- INCREASED SIZE and GYRATION (ROTATION)
- FISSURE FORMATION
- VENTRICULAR ENLARGEMENT
- 4X INCREASE in CORTICAL GREY MATTER from 20 WEEKS
- NOCICEPTION from 21 WEEKS (sensory, cant detect painful stimuli)
when does NOCICEPTION (sensory, detect stimuli) begin
21 WEEKS
how much INCREASE in BRAINS CORTICAL GREY MATTER from 20 WEEKS
4X
FETAL GROWTH is LINEAR until
20 WEEKS
how ACCURATE are ULTRASOUNDS at detecting size of fetus
40-50%
Symphysial Fundal Height: 25-35%
however correlation of fetal size with pathology is poor
CAUSES of FETAL OVERGROWTH (growth > 95th percentile)
(common)
- mostly IDIOPATHIC (NO IDENTIFIABLE CAUSE)
- DIABETES
- FETAL OVERGROWTH SYNDROMES
FETAL GROWTH RESTRICTION (Failure to achieve genetic growth potential) PATHOLOGICAL CAUSES:
(can still be small and healthy unless FGR)
- PLACENTAL functioning
- INFECTIONS (CMV etc)
- GENETIC/CHROMOSOMAL problems
- potentially Starvation of mother
QUICKENING of FETAL MOVEMENTS are when
16-20 WEEKS
more than 80% of time will be asleep
more active at night - diurnal rhythm
Reduction/Loss of fetal movements may be pathological
how is LUNG DEVELOPMENT
CONTINUOUS from 4th week (from splanchnic mesoderm)
Critical period: 16-24
can see FETAL BREATHING FROM 20 WEEKS
increases from 15 to 30% in 3rd trimester
when do ALVEOLI of LUNGS DEVELOP
AFTER 24 WEEKS
further development after birth from 100 million to 300 million
in LUNG DEVELOPMENT what do TYPE 2 PNEUMOCYTES PRODUCE from 28 WEEKS
in what phase
what does it prevent
SURFACTANT (PHOSPHOLIPID)
in SACCULAR PHASE
- PREVENTS ALVEOLAR COLLAPSE
FETAL RESPIRATORY CHANGES at BIRTH
- LUNGS INFLATE and FILL with air, PUSHING AMNIOTIC FLUID OUT of lungs
- INCREASED FETAL OXYGENATION
- this causes DECREASES in BLOOD FLOW RESISTANCE
what does SURFACTANT in LUNGS do
REDUCES SURFACE TENSION of ALVIOLI
- AIDS BREATHING
- PREVENTS ALVELOAR COLLAPSE
how is FETAL HAEMOGLOBIN (HbF) in comparison to ADULT HEAMOGLOBIN
HIGHER AFFINITY for OXYGEN
so HIGHER AMOUNT of circulating Haemoglobin (16-18 g/dl)
(adult : 11-15 g/dl)
(HgF makes up 90% of fetuses haemoglobin)
important BYPASSES in FETAL LUNGS
- DUCTUS ARTERIOSIS
connects pulmonary artery and aorta - FORAMEN OVALE ( allows right to left shunt)
have HIGHER VASCULAR RESISTANCE
how is FETAL CIRCULATION
relative HYPOXIA (low oxygen levels)
pH 7.25
MIXED OXYGENATION
at BIRTH how does fetal circulation CONVERT to ADULT CIRCULATION
- LOWER PULMONARY OXYGENATION
- LOWER VASCULAR RESISTANCE
- FORAMEN OVALE CLOSES
- DUCTUS ARTERIOSUS CLOSES
increased oxygenation
Haemolysis over weeks to compensate
is FETAL HAEMOGLOBIN higher or lower than ADULT HAEMOGLOBIN
HIGHER (16-18 g/dl)
(adult 11-15 g/dl)
with HIGHER AFFINITY
FETAL DISORDERS include what types of abnormalities
CHROMOSOMAL, GENETIC and STRUCTURAL anomalies of fetus
FETAL ANOMALIES can occur in approx how many pregancies
2-3%
examples of ANEUPLOIDY FETAL ANOMALIES
- Down syndrome (Trisomy 21)
- Turner Syndrome (1 X chromosome)
- Trisomy 13 aka Patau’s
- Trisomy 18 aka Edward’s
examples of GENETIC CONDITIONS in FETAL ANOMALIES
- Beckwith-Weideman
- Fragile X Syndrome
examples of STRUCTUAL FETAL ANOMALIES
- Cardiac
- Neurological
- Skeletal
- Genetic
- Thoracic
- Renal/Urological
CHARACTERISTICS of DOWN SYNDROME (TRISOMY 21)
- ADDITIONAL CHROMOSOME 21 (3 copies)
- INCURABLE
- MENTAL impairment
- CARDIAC disorders
- Characteristic FEATURES
many require lifelong care (but varies)
what can DOWN SYNDROME be related to
MATERNAL AGE at conception
- more likely in older women
(especially increases after 40)
94% of TRISOMY 21 is due to
NON-DISJUNCTION
failure of sister chromosomes to divide equally during cell division
leads to oocyte with 2 copies of chromosome 21 (instead of haploid)
with sperm becomes 3 copies of chr. 21
other GENETIC CAUSES of TRISOMY 21 (less common)
- 2.4% MOSAICISM
after fertilisation.
some cells have 3 chr. 21, some don’t
characteristics vary - 3.3% ROBERTSONIAN TRANSLOCATION
correct number in a parent but different arrangement of chr. 21
methods of SCREENING for TRISOMY 21
- BIOCHEMICAL TESTS (triple or quad) (biochemical markers)
- look at NUCHAL TRANSLUCENCY
- COMBINED TEST (biochemical and nuchal)
- INTEGRATED TEST
- NON-INVASIVE PRENATAL TEST (free foetal DNA)
(diagnostic: invasive test , CVS or amniocentesis)
screening for FETAL ANATOMY
FETAL STRUCTURAL ANOMALY SCREENING
RISK FACTORS for CARDIAC DISORDERS in FETUS
- FAMILY HISTORY
- DIABETES
- CHROMOSOMAL problems history
- GENETIC problems history
- DRUGS
examples of DEFECTS seen in FETAL CARDIAC DISORDERS
- VALVULAR defects
- SEPTAL defects
- VENTRICULAR defects
- OUTFLOW TRACTS defects
NEUROLOGICAL DISORDERS
often SEVERE
related to NEURODEVELOPMENTAL DELAY and CEREBRAL PALSY
might see:
Ventriculomegaly (ventricle enlargement)
cerebellar
loss of sulcation/gyration
bleeds
example of a NEURAL TUBE DEFECT (FAILURE TO CLOSE)
SPINA BIFIDA
risk reduced by folic acid
what is MICROCEPHALY and what are causes
FAILURE of BRAIN and SKULL to GROW
associated with MENTAL IMPAIRMENT
CAUSES: VIRAL (ZIKA virus), CHROMOSOMAL. CRANIOSYNOSTOSIS (sutures fuse premature), ALCOHOL, DRUGS
SKELETAL DISORDERS includes having
- MISSING BONES
- ABNORMAL SHAPE of BONES
- MINERALISATION problems
- FRACTURES
CRANIO-FACIAL PROBLEMS
- CLEFT LIP and PALATE (corrective surgery)
GASTROINTESTINAL DISORDERS
- ECHOGENIC BOWEL
(genetic, CMV, Cystic Fibrosis)
ABDOMINAL WALL DEFECTS:
- GASTROSCHISIS
bowel/liver outside of abdomen, doesn’t return after herniation
- OMPHALOCELE
herniation covered with Peritoneum
(can be chromosomal disorders)
RENAL DISORDERS include KIDNEYS that are:
- ABSENT
- UNILATERAL (one side)
- WRONG POSITION
- abnormal looking - CYSTIC or FAILURE to DEVELOP CORRECTLY
serious if both kidneys
RENAL DISORDERS can also include BLADDER problems (less common, more common in boys)
DRUG RELATED problems from which DRUGS
- THALIDOMIDE (given for morning sickness)
caused severe malformations in fetus,
underdeveloped upper limbs - ANTIEPILEPTICS
eg SODIUM VALPROATE (10%)
can cause Spina Bifida, Cleft Palate, Cardiac defects
is SCREENING for TRISOMY 21 100% effective
NO
most accurate is non-invasive
Biochemical
TRIPLE (69%)
QUAD (81%
NUCHAL TRANSLUCENCY (80%)
COMBINED (82-87%)
INTEGRATED (96%)
which GASTROINTESTINAL DISORDER is related to CHROMOSOMAL DISORDERS
OMPHALOCELE - herniation covered with peritoneum
NOT gastroschisis (bowel/liver outside abdomen)