Aging&Development Flashcards
define fertilisation age
1 day after last ovulation
measured from time of fertilisation
define gestational age
calculated from the time of beginning of last menstrual period
what is Carnegie staging?
23 stages of embryo development
based on embryo features, not time
covers 0-60 day fertilisation age
when does the embryogenic stage occur?
14-16 days post fertilisation
what happens at the embryogenic stage?
the early embryo is differentiated from the fertilised oocyte
two populations of cells - pluripotent embryonic cells and extraembryonic cells
when does the embryonic stage occur?
16-50 days post fertilization
what defines the embryonic stage?
germ layers
differentiation of tissue types
body plan established
when does the fetal stage occur?
50-270 days post fertilization, i.e second and third trimester
what defines the fetal stage?
presence of major organs
migration of organs to final location
growth
acquisition of metal viability
name the stages from fertilised oocyte to the 200/300 cell structure
what is present at all stages?
1 cell zygote → cleavage stage embryos (2-8cells) → morula 16+ cells → blastocyst
zona pellucida
what is the maternal zygotic transition?
when does it happen?
embryo is dependent on maternal mRNA & proteins (made in oocyte development) until 4-8 cell stage
here embryogenic genes are transcripted (zygotic genome activation) → ↑ protein synthesis and organelle maturation
what is compaction? when does it occur?
outer cells of embryo are pressed against zone and become wedge shaped
outer cells connect via gap junctions and desmosomes → diffusion barrier between inner and outer embryo
outer cells are polarised
occurs after 8-cell stage
what happens to the blastocyst after compaction?
inner cells reorganise to one side to form the blastocoel cavity
what is the blastocoel? how is it formed?
fluid filled cavity
trophoblast pumps sodium ions into it and water osmotically follows
what are 2 functions of the zone pellucida?
prevents polyspermy
protects early embryo
what cells does the inner cell mass consist of?
pluripotent embryonic cells (contribute to final organism)
what is the trophoectoderm? what cells does it consist of?
outer cell layer - extra-embryonic cells i.e. trophoblasts (contribute to structures supporting development)
what is hatching? when and how does it occur?
when the embryo escapes the zone pellucida
at day 5-6
cellular contractions and enzymatic digestions
what happens in peri-implantation events?
@ day 7-9
trophoblasts → syncitiotrophoblasts & some cytotrophoblasts remain
inner cell mass → epiblast and hypoblast
what is the function of syncitiotrophoblasts and cytotrophoblasts?
destroy maternal endometrial cells to create interface between embryo and maternal blood supply
cytotrophoblasts remain to provide source of syncitiotrophoblasts
what do syncitiotrophoblasts secrete?
hcg - human chorionic gonadotrophin
what will the epiblast and hypoblast form?
epiblast → fetal tissues
hypoblast → yolk sac
what is the bilaminar embryonic disc formation? when does it occur?
day 12+
some epiblast cells become separated when the amniotic cavity is formed
cells above → amnion → extra-embryonic membranes
(picture from bottom to top : cytotrophoblast → blastocoel → hypoblast → epiblast → amniotic cavity → amnion → cytotrophoblasts dividing → syncitiotrophoblast → invading maternal endometrium)
what is gastrulation? when does it occur?
15 days post-fertilisation
1. primitive streak forms through epilblast → divides embryo into cranial and caudal ends (and L&R) with primitive pit in the centre and primitive groove towards caudal end
2. epiblast cells invaginate through streak and displace hypoblast cells
hypoblast cells → endoderm
epiblast cells → ectoderm
cells in between → mesoderm
name 5 organs the endoderm forms?
GI tract pancreas liver lung thyroid
name 3 things the ectoderm forms?
tooth enamel
CNS/neural crest
skin epithelia
name 7 things the mesoderm forms?
blood muscle cartialage bone kidenys adrenal cortex gonads
what is the notochord? when and where does it form?
tube structure formed of cartilage like cells
key organising centre for neurulation and ,mesoderm development
forms under ectoderm along embryo midline at ~day13+
explain the process of neurulation
- the notochord signals the neural plate ectoderm to invaginate and form a neural groove
- two neural folds from along the cranio-caudal axis
- neural crest cells form in neural folds
- neural folds move together over neural groove and fuse → hollow neural tube (surrounded by ectodermal epidermis)
- neural crest cells migrate out of neural folds to differentiate
- closure at head end ~day 23 , closure at tail end ~day27
what condition arises when the neural tube fails to close at the head end?
anencephaly
what condition arises when the neural tube fails to close at the tail end?
spina bifida
what germ layer do neural crest cells come from?
ectoderm
name some structure neural crest cells differentiate into
cranial - neurones, ossicles, lower jaw
cardiac - aortic arch
trunk - sympathetic ganglia, adrenal medulla, melanocytes
vagary & sacral - parasympathetic ganglia, enteric NS ganglia
what defects can neural crest differentiation failure lead to?
pigmentation disorders
deafness
cardiac/facial defects
no gut innervation
what is somitogenesis? where does it occur?
formation of somites, commences at head of neural tube down long axis of embryo
how do somites form?
arise from paraxial blocks of mesoderm along the neural tube and notochord
what tissues do somites form?
sclerotome - vertebrae and tip cartilage
dermomyotome → dermatome (dermis, fat & connective tissue) & myotome (muscles)
when and how does the gut tube form?
~day 16 +
embryo folds laterally and ventrally to pinch off part yolk sac → primitive gut (fore, mid & hindgut)
what structures do each the fore, mid and hingut consist of?
fore - oesophagi, stomach, 1st part of duodenum, liver, pancreas, gallbladder
mid - remaining duodenum, jejunum, ileum, ascending colon, proximal 2/3s of transverse colon
hind - distal 1/3 transvers colon, descending colon, rectum, anal canal
what germ layer does the heart form from? when does this occur?
mesoderm ~day 19
beating and pumping blood ~day 22
around when can you detect a fetal heartbeat?
6 weeks gestational age
from what and when do the lungs form?
the lung bud (endoderm) in the 4th week
what germ layer do the gonads form from? what are the initial structures called?
mesoderm
bipotenital gonadal ridges (bipotential = not committed to testis or ovaries)
how do testis and ovary development differ?
XY embryo - presense of SRY gene directs gonadal cells → Sertoli cells → testis formation, leydig cells, testosterone production
XX embryo - absence of SRY → gonadal cells → granulosa cells → ovary development (reinforcement from FOXL2)
what are the 3 broad causes of early pregnancy loss?
errors in embryo foetal development
failure of embryo to implant in uterine lining
inability to sustain development of implanted embryo
define miscarriaage
loss of pregnancy prior to 23 weeks gestation
<12 weeks → early clinical pregnancy loss
12-24 weeks → late clinical pregnancy loss
what percentage of conceptions result in preclinical loss? what does this mean?
60 percent
preclinical means the pregnancy was undetectable, i.e. before a missed menstrual period
what is the likely major cause of early pregnancy loss?
aneuploidy
why does aneuploidy increase with maternal age?
prolonged meiotic arrest in oocytes (prophase I)
homologous chromosomes are held together via cohesin proteins
there is a loss of cohesin with age leading to loss of cohesion between homologous chromosomes
lost cohesion → chromatids can separate and drift during meiotic division → inaccurate spindle segregation → aneuploidy
name 2 cohesin proteins
REC8
SMC2
maintain cohesion between chromatids
how is recurrent miscarriage/pregnancy loss defined in the UK?
three or more pregnancy losses (consecutive or not)
reduced levels of what might contribute to RPL/RM?
LIF in uterine secretions
what aspects do the maternal and paternal genomes contribute to embryo viability?
maternal - restrict embryo fitness to conserve resources for future pregnancies
paternal - promote embryo fitness at expense of mother
what are gestational trophoblastic diseases characterised by?
overgrowth of trophoblastic tissue
what are the benign causes of gestational trophoblastic diseases?
complete and partial hydatidiform moles
what are the malignant causes of gestational trophoblastic diseases?
neoplasias (some arising from hydatidiform moles)
- invasive moles
- choriocarinoma
- placental site trophoblastic tumour
- epithelioid trophoblastic tumour
what is the difference between a complete and partial hydatidiform mole?
complete = no fetal tissue present
how does a complete hydatidiform mole arise?
empty egg fertilised by two sperm cells or by one sperm cell that’s genome duplicates
how does a partial hydatidiform mole arise?
a normal egg is fertilised by two sperm cells or by one sperm cell that’s genome duplicates
what mutations may underly recurrent hydatidiform moles?
NLRP7 mutations
what is an ectopic pregnancy?
implantation of embryo at site other than uterine endometrium (normally Fallopian tube)
what component of cigarette smoke is thought to contribute to ectopic pregnancy?
continine
how is continine thought to contribute to ectopic pregnancy? 2 ways
it up regulates the expression of the PROKR1 receptor in the Fallopian tubes - this is thought to hinder contractility and hence the transfer of the egg to the womb
it induces pro-apoptosis protein expression in the Fallopian tube
how is cannabis thought to cause ectopic pregnancy? 2 ways
tHC components may act on the Fallopian tube and perturb embryo transit
OR
alter the endocannabinoid balance in the fT → disrupted embryo environment
what receptors are reduced in ectopic pregnancy patients?
cannabinoid receptors CB1
10 risk factors for ectopic pregnancy?
previous ectopic pregnancy prior ft surgery STIs endometriosis pelvic inflammatory disease cigarette smoking cannabis use ≥35 yrs history of infertility IVF
what is the non-selective uterus hypothesis?
the uterus allows implantation if poor quality embryos due to changes in uterine mucus expression in women with RPL/RM
pregnancy is detectable but not sustainable
Outline the two types of embryo/foetus nutrition
T1 - histiotrophic - embryo relies on uterine gland secretions and endometrial tissue/capillaries breakdown
T2→term - haemotrophic - maternal blood directly contacts foetal membranes via haemochorial type placenta
what kind of placenta do humans have?
haemochorial-type
what’s the function ofnthe connecting stalk?
links embryo to chorion
what are trophoblastic lacunae?
spaces formed by breakdown of capillaries and uterine glands, filled with maternal blood → intervillous/maternal blood spaces
what are fetal membranes? name them
extra-embryonic tissues that forma tough flexible sac encapsulating the foetus
forms basis of maternal-fatal interface
amnion - inner
chorion - outer
what is the amnion?
inner fetal membrane
arises from epiblast
closed avascular sac with embryo at one end
secrets amniotic fluid from 5th week → fluid sac that surrounds and protects foetus
when does amniotic fluid start being secreted?
from the 5th week
what is the chorion?
outer fetal membrane
formed from yolk sac and trophoblast
v vascularized
forms chorionic villi
what are chorionic villi?
outgrowths of cytotrophoblast from chorion
project through syncitiotrophoblast into maternal endometrium
form basis of fetal side of placenta
differences between amnion and chorion
amnion = inner, avascular, epiblast chorion = outer, highly vascular, yolk sac and trophoblast
what is the allantois?
yolk sac outgrowth
forms along connecting stalk from embryo to chorion
forms umbilical cord
what does the allantois become and how?
umbilical cord
becomes coated in mesoderm and vascularises
how does the amniotic sac form?
the expanding amnion is forced into contact with the chorion and they fuse to form the sac
what is the function of chorionic villi?
provide surface area for the exchange of gases and nutrients
outline the 3 phases of chorionic villi development
primary - cytotrophoblast outgrowth and branching of these extensions
secondary - growth of fetal mesoderm into primary villi
tertiary - growth of umbilical artery and vein into villus mesoderm
explain the terminal villus microstructure and how its suited to function?
convuluted knot of vessels and vessel dilation (coated in trophoblast)
→ slows blood flow to allow exchange between maternal and fetal blood
how do the terminal chorionic villi change from early to late pregnancy?
villi initially thick with thick layer of trophoblast between capillaries and maternal blood
villi and trophoblast layer then thin and separation form maternal blood reduces
outline the succession of maternal blood supply to the endometrium
uterine artery → arcuate → radial → basal → spiral (arise during menstrual cycle endometrial thickening)
which arteries supply blood to endometrium?
spiral arteries
outline the process of conversion (i.e. spiral artery remodelling)
extra-villus trophoblast cells coating villi invade spiral arteries to form endovascular EVT (breakdown and replace maternal endothelium) → converts spiral artery into low pressure high capacity conduit for maternal blood flow
how is oxygen transported across the placenta?
via diffusional gradient - high maternal oxygen tension and low fetal tension
how is glucose transported across the placenta?
facilitated diffusion by transporters on maternal side and foetal trophoblast cells
how is water transported across the placenta?
mostly diffusion
some local hydrostatic gradients
how are electrolytes transported across the placenta?
diffusion
active co-transport
how is calcium transported across the placenta?
actively transported via magnesium ATPase calcium pump
how are amino acids transported across the placenta?
active transport
what are some maternal cardiorespiratory changes that occur?
increased cardiac output 30%
decreased peripheral resistance 30%
increased blood volume 40%
increased pulmonary ventilation 40%
how is foetal oxygen content and saturation similar to maternal blood?
even though fetal oxygen tension (partial pressure) is low , fetal Hb has a higher affinity for oxygen than maternal Hb
what is the site of gas exchange for the foetus?
placenta
how do ventricles pump in the foetus? why?
parallel instead of series → ↑ efficiency
how are the fetal pulmonary and hepatic circulations bypassed?
via vascular shunts that close at birth
what happens to the fetal respiratory system at ~20weeks?
primitive air sacs form and surfactant production begins
vascularisation at ~28weeks
what is the theory behind fetal rapid respiratory movements?
1-4hr/day during REM sleep
thought to be breathing practice and to develop diaphragm
when does the fetal endocrine pancreas start to be functional?
from start of 2T , insulin produced from mid-2T
what is meconium?
first stool passed after birth
formed from digested amniotic fluid containing debris and bile acids
when do foetal movements begin?
late 1T, detectable by mothers at ~14 weeks
from when can the foetus respond to stress?
18 weeks
when do foetal thallus-cortex connections form?
24 weeks
what sleep is the foetus mostly in?
slow wave or REM
How is labour similar to a pro-inflammatory reaction?
immune cell infiltration
inflammatory cytokine and prostaglandin secretion
what are the 4 phases of parturition?
1 - quiescence - cervical softening
2 - activation - cervical ripening
3 - stimualtion - uterine contraction, cervical dilation, fetal and placenta expulsion
4 - involution - uterine involution, cervical repair, breast feeding
what are the 3 stages of Labour? (phase 3)
1 - contractions begin and cervix dilates
- latent phase : slow cervix dilation to 2-3cm
- active phase : rapid dilation to 10cm
2 - delivery of foetus - fulll dilation and maximal myometrial contractions
3 - placenta delivery and foetal membranes , postpartum repair
how long are deliveries usually?
first - 8-18 hours
subsequent - 5-12 hours
what is the function of the cervix? how does its strcuytuee support this?
retaining foetus in uterus
high connective tissue content (collagen fibres embedded in proteo-glycan matrix) provide rigidity and stretch resistance
how does the cervix remodel throughout pregnancy?
Softening ~1T (changes in compliance but retina competence)
Ripening a few weeks before birth - monocyte infiltration, IL-6 & 8 secretion, hyaluron deposition
Dilation to increase elasticity - increased hyaluronidase to breakdown hyaluron , matrix metalloproteinases decrease collagen content
Post-partum repair - restore tissue integrity and competency
what’s the theory behind the initiation of labour?
determined by foetus through changes in HPA axis
foetal CRH levels rise exponentially towards end of pregnancy
reduced amount of CRH binding protein → CRH bioavailability increases
what are the functions if CRH in labour?
↑ foetal CRH → ↑ ACTH →↑ cortisol
cortisol drives placental production of CRH → ↑ foetal cortisol (positive feedback)
CRH stimulates DHEAS production byu fetal adrenal cortex → oestrogen substrate
why is progesterone high during pregnancy?
maintains uterine relaxation
how do uterine receptors change as term approaches?
switch from PR-A activating isoforms to repressive PR-B and PR-C isoforms in the uterus
→ functional progesterone withdrawal
rise in oestrogen receptor Alpha expression
=uterus becomes blinded to progesterone action and sensitised to oestrogen action
=chnage in E:P ratio in favour of oestrogen
what type of hormone is oxytocin and where is synthesized?
nonapeptide hormone
utero-placental tissues and pituitary
what happens to uterine oxytocin levels at labour onset?
sharply increase due to increase in oestrogen levels
release promoted by the Ferguson reflex
what is the Ferguson reflex?
foetal distension of cervix and vagina activates stretch receptors → impulses conveyed to paraventricular and supraoptic nuclei in hypothalamus → ↑ firing rate to posterior pituitary → ↑ oxytocin release
through which receptor does oxytocin signal?
G-coupled oxytocin receptor OTR/OXTR
what inhibits OXTR expression pre-labour? how does this change in labour?
progesterone
↑ oestrogen → ↑↑ in uterine oxtr expression
what are the functions of oxytocin?
increases myocyte connectivity in myometrium by increasing no. gap junctions → syncytium
destablise membrane potentials to lower threshold for contraction
enhances liberation of intracellular calcium ion stores
what are the 3 primary prostaglandins secreted in labour?
PGE2
PGF2 alpha
PGI2
what promotes increased prostaglandin action?
↑ estrogen → activates phospholipase A2 enzyme → ↑ arachidonic acid → ↑ PG synthesis
↑ oestrogen → ↑ oxtr expression → ↑ PG release
what is the fucntion of PGE2?
cervix remodelling
- leukocyte infiltration into cervix, IL-8 release , collagen bundle remodelling
what is the fucntion of PGI2?
myometrium
- promotes myometriral smooth muscle relaxation and lower uterine segment relaxation
what is the fucntion of PGF2 alpha?
myometriol contractions
- works w oxytocin to destabilise membrane potentials and promote myocyte connectivity
what 2 other factors are involved in cervix remodelling?
relaxin
nitric oxide
outline myometrial contractions during labour
start from fundus and spread down upper segment to lower segement
contractions are brachystatic → fibres do not return to full length on relaxation
causes lower segment and cervix to pull up to form birth canal
what happens in the final phase of labour?
uterus shrinks
→ after delivery area of contact with placenta and endometrium reduces
→ folding of fetal membranes → peel off endometrium
umbilical cord clamped → stops fetal blood flow to placenta → villi collapse → hematoma forms between decidua and placenta
contractions expel placent abd foetal tissues
why does the uterus remain in a contracted state after delivery?
facilitate uterine vessel thrombosis and healing of those vessels and to prevent intrauterine bleeding → uterus restoration and cervix repair
why is cervix repair and uterus restoration important?
to prevent commensurate bacteria entering uterus
restore endometrial cyclicity in response to hormones to allow implantation of another embryo
how is pre-eclampsia diagnosed?
new onset hypertension in previously normotensive woman, after 20wks gestation
SBP ≥ 140
OR
DBP ≥90
signs and symptoms of pre-eclampsia?
reduced foetal movement ↓ amniotic fluid oedema headache abdo pain visual disturbances, seizures, breathlessness
2 subtypes of preeclampsia? and associated symptoms?
early onset - <34wks, fetal and maternal symptoms, changes in placental structure
late onset - ≥34wks , mainly maternal symptoms, fewer placental changes
risk factors for preeclampsia?
maternal age ≥40/≤20 family history autoimmune conditions, diabetes, pcos, renal disease bmi ≥ 30 previous (gestational) hypertension
what are the risks of preeclampsia?
damage to maternal kidneys, brain, liver etc
progression to eclampsia - seizures
placental abruption
reduced foetal growth, preterm birth, loss/stillbirth
what happens in preeclampsia that differs from normal pregnancy?
the EVT invasion of spiral arteries is limited to the decimal layer (normally extends into smooth muscle and endothelium) → spiral arteries not remodelled as much → less capacity → ↓ placental perfusion
what factors does a healthy placenta normally release and their function?
VEGF and placental growth factor (PLGF) - pro-angiogenic
normally bind to (s)Flt1 (VEGFR1) to limit their bioavailability
when bound on endothelial cells → anticoagulant and vasodilatory
how does a distressed placenta differ in preeclampsia in terms of factors released?
releases more soluble VEGFR1/Flt1 → less bioavailability of pro-angiogenic PLGF and Vegf → endothelial dysfunction
less PLGF/VEGF bound to Flt-1 on endothelial membrane = ↑ procoagulant & vasoconstriction
what can be measured to predict PE onset?
PLGF levels for triage , ≤100 abnormal, ≤12 highly abnormal (↑risk for preterm delivery), (20-37 wks)
sFlt-1/PlGF ratio (24 - 37 weeks), ≥38 is abnormal
what is the only way to resolve preeclampsia?
delivery of the placenta
managemen options for PE?
≤34wks - try maintain pregnancy
≥37wks - delivery preferable
anti-hypertensives
corticosteroids for ≤34 wks to promote lung development
how can PE be prevented?
weight loss
exercise throughout pregnancy
low dose aspirin for high risk groups
what can PE increase the risk of devloping?
T2DM
renal disease
CVD
preeclampsia in next pregnancy
what factors can affect a foetus that could have a lasting effect?
maternal nutrition, illness, stress, medication
fetal infection in utero
environmental exposures
what is the barker hypothesis?
adult health is somewhat determined by early life factors/intrauterine environment
eg. undernutriiton in utero & overnutrition as a child → ↑ risk of metabolic syndrome (CVD, T2DM, stroke)
DOHaD proposed mechanism?
intrauterine environment leads to epigenetic changes which influence development and physiology
what is epigenetic?
heritable changes in marks on DNA that dont change nucleotide sequence but influence how genes are expressed
outline the NHS healthy child programme?
universal
aims to reduce health inequalities, prevent disease and promote good health
key : obesity prevention
support care givers
screening
immunisation
identify high risk people for additional support
signposting for accident prevention and dental hygiene
3 examples of early childhood screening?
newborn check
newborn hearing sceren
blood spot check (heel prick test)
what are the fundamentals for a good screening test?
disease should be identifiable before critical point, treatable and it should prevent / ↓ mortality/morbidity
easy to administer
cost effective
reproducible with accurate results
name a programme being used to optimise early life outcomes
Sure Start
name an NHS screening test undertaken preconception?
diabetic eye screening for women with T1DM/T2DM
name an NHS screening test undertaken in trimester 1?
early scan/blood test for T21, T18 and T13 screening
name an NHS screening test undertaken in trimester 2/3?
detailed ultrasound for structural abnormalities, T18 and T13
another diabetic eye screen for women with diabetes
name an NHS screening test undertaken in a newborn?
hearing screen
blood spot screens for SCD, CF, hypothyroidism, inherited metabolic diseases
what are the primitive reflexes of gross motor development?
Moro Reflex - let neck go and arms will abduct then adduct, should go at 3-6mths
Standing Reflex until 3 months, extend legs
Grasp Reflex - grasp objects, stoke side of palm → open
Parachute reflex - tilt forward, outstretch arms to protect, 6-9mths
what are the 4 domains of child developmental assessment?
fine motor
gross motor
social
speech & language
what should be observed in the pull to sit movement?
the baby’s head should not lag and it should be able to hold it upright (6/7 months)
what are the sitting milestones for babies?
6 months - sitting unsupported with round back
8 months - sitting unsupported with straight back
what gross motor development should be observed at 6-8wks?
raising head to 45º whilst on tummy
when should a baby be able to roll over?
3-5mths
when should a baby start crawling and standing w cruising around furniture?
8-9mths
10 mths
what are the walking milestones for babies?
12 months - unsteady broad gait
15 months - steady walk
variations of normal crawling?
bottom shuffle
commando crawl
crawling on all 4s
what are the vision milestones for babies?
6wks - follow moving object by turning head
4 months - reaching out for toys
what are the fine motor milestones for babies?
4-6 months - palmar grasp 7 months - move toys from one hand to other 10 months - mature pincer grip 16-18months - marks w crayon 14months-4yrs - tower building 2-5yrs - drawing shapes
when should a baby startle to loud noises?
newborn
when should a baby start vocalising?
3-4mnths
when should a baby turn to soft sounds?
7motnhs
when should polysyllabic babble start?
7-10months
baby language milestones?
coos/laughs - 4 months polysyllabic babble - 7-10months words other than mama/dada - 12 months 6-10 words - 18months simple phrases - 20-24 months sentences - 2.5-3yrs
when should a baby start smiling?
6 weeks
when should a baby be able to feed/drink itself?
6-8months using hands
12 months drinking from cup w 2 hands
18 months with holding spoon
symbolic play and parallel play age?
18-24 mths
2.5-3 years
potty trained age?
2years
what are the patterns of abnormal development?
slow but steady
plateau
regression
4 main gross motor developments and limit ages ?
head control - 4months
sits unsupported - 9 months
stands independent - 12 months
walks independently - 18 months
4 main vision and fine motor developments and limit ages ?
fixes and follows visually - 3 months
reaches for objects - 6 months
transfers - 9 momnths
pincer grip - 12 months
4 main hearing, speech & language developments and limit ages ?
polysyballbi babble - 7 monmths consonant babble - 10 months 6 words with meaning - 18 months joins work - 2 years 3 word sentences - 2.5 years
4 main social/emoptional behaviour developments and limit ages ?
smiles - 8 weeks fear of strangers - 10 months feeds self w spoon - 18 months symbolic play - 2-2.5 years interactive play - 3-3.5 years
who and when should a baby’s development be monitored?
parents, teachers, doctors, nurses
oppurtunistically
as part of the healthy child programme
what 4 principles underpin the healthy child programme?
screening
immunisation
child health reviews
health promotion
what can contribute to a delayed development?
ill health
lack of physical/psychological stimuli
seneory/motor impairment
reduced inherent potential
types of developmental delay?
global eg. downs syndrome, drugs, infections
specific -
- language eg. hearing loss, autism
- motor eg. cerebral palsy
- sensory
- cognitive
