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BRS 2 > Aging&Development > Flashcards

Aging&Development Flashcards

1
Q

define fertilisation age

A

1 day after last ovulation

measured from time of fertilisation

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2
Q

define gestational age

A

calculated from the time of beginning of last menstrual period

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3
Q

what is Carnegie staging?

A

23 stages of embryo development
based on embryo features, not time
covers 0-60 day fertilisation age

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4
Q

when does the embryogenic stage occur?

A

14-16 days post fertilisation

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5
Q

what happens at the embryogenic stage?

A

the early embryo is differentiated from the fertilised oocyte
two populations of cells - pluripotent embryonic cells and extraembryonic cells

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6
Q

when does the embryonic stage occur?

A

16-50 days post fertilization

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7
Q

what defines the embryonic stage?

A

germ layers
differentiation of tissue types
body plan established

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8
Q

when does the fetal stage occur?

A

50-270 days post fertilization, i.e second and third trimester

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9
Q

what defines the fetal stage?

A

presence of major organs
migration of organs to final location
growth
acquisition of metal viability

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10
Q

name the stages from fertilised oocyte to the 200/300 cell structure
what is present at all stages?

A

1 cell zygote → cleavage stage embryos (2-8cells) → morula 16+ cells → blastocyst
zona pellucida

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11
Q

what is the maternal zygotic transition?

when does it happen?

A

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

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12
Q

what is compaction? when does it occur?

A

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

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13
Q

what happens to the blastocyst after compaction?

A

inner cells reorganise to one side to form the blastocoel cavity

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14
Q

what is the blastocoel? how is it formed?

A

fluid filled cavity

trophoblast pumps sodium ions into it and water osmotically follows

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15
Q

what are 2 functions of the zone pellucida?

A

prevents polyspermy

protects early embryo

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16
Q

what cells does the inner cell mass consist of?

A

pluripotent embryonic cells (contribute to final organism)

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17
Q

what is the trophoectoderm? what cells does it consist of?

A

outer cell layer - extra-embryonic cells i.e. trophoblasts (contribute to structures supporting development)

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18
Q

what is hatching? when and how does it occur?

A

when the embryo escapes the zone pellucida
at day 5-6
cellular contractions and enzymatic digestions

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19
Q

what happens in peri-implantation events?

A

@ day 7-9
trophoblasts → syncitiotrophoblasts & some cytotrophoblasts remain
inner cell mass → epiblast and hypoblast

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20
Q

what is the function of syncitiotrophoblasts and cytotrophoblasts?

A

destroy maternal endometrial cells to create interface between embryo and maternal blood supply
cytotrophoblasts remain to provide source of syncitiotrophoblasts

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21
Q

what do syncitiotrophoblasts secrete?

A

hcg - human chorionic gonadotrophin

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22
Q

what will the epiblast and hypoblast form?

A

epiblast → fetal tissues

hypoblast → yolk sac

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23
Q

what is the bilaminar embryonic disc formation? when does it occur?

A

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)

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24
Q

what is gastrulation? when does it occur?

A

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

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25
Q

name 5 organs the endoderm forms?

A 
GI tract
pancreas
liver
lung
thyroid
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26
Q

name 3 things the ectoderm forms?

A

tooth enamel
CNS/neural crest
skin epithelia

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27
Q

name 7 things the mesoderm forms?

A 
blood
muscle
cartialage
bone
kidenys
adrenal cortex
gonads
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28
Q

what is the notochord? when and where does it form?

A

tube structure formed of cartilage like cells
key organising centre for neurulation and ,mesoderm development
forms under ectoderm along embryo midline at ~day13+

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29
Q

explain the process of neurulation

A
  1. the notochord signals the neural plate ectoderm to invaginate and form a neural groove
  2. two neural folds from along the cranio-caudal axis
  3. neural crest cells form in neural folds
  4. neural folds move together over neural groove and fuse → hollow neural tube (surrounded by ectodermal epidermis)
  5. neural crest cells migrate out of neural folds to differentiate
  6. closure at head end ~day 23 , closure at tail end ~day27
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30
Q

what condition arises when the neural tube fails to close at the head end?

A

anencephaly

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31
Q

what condition arises when the neural tube fails to close at the tail end?

A

spina bifida

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32
Q

what germ layer do neural crest cells come from?

A

ectoderm

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33
Q

name some structure neural crest cells differentiate into

A

cranial - neurones, ossicles, lower jaw
cardiac - aortic arch
trunk - sympathetic ganglia, adrenal medulla, melanocytes
vagary & sacral - parasympathetic ganglia, enteric NS ganglia

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34
Q

what defects can neural crest differentiation failure lead to?

A

pigmentation disorders
deafness
cardiac/facial defects
no gut innervation

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35
Q

what is somitogenesis? where does it occur?

A

formation of somites, commences at head of neural tube down long axis of embryo

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36
Q

how do somites form?

A

arise from paraxial blocks of mesoderm along the neural tube and notochord

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37
Q

what tissues do somites form?

A

sclerotome - vertebrae and tip cartilage

dermomyotome → dermatome (dermis, fat & connective tissue) & myotome (muscles)

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38
Q

when and how does the gut tube form?

A

~day 16 +

embryo folds laterally and ventrally to pinch off part yolk sac → primitive gut (fore, mid & hindgut)

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39
Q

what structures do each the fore, mid and hingut consist of?

A

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

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40
Q

what germ layer does the heart form from? when does this occur?

A

mesoderm ~day 19

beating and pumping blood ~day 22

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41
Q

around when can you detect a fetal heartbeat?

A

6 weeks gestational age

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42
Q

from what and when do the lungs form?

A

the lung bud (endoderm) in the 4th week

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43
Q

what germ layer do the gonads form from? what are the initial structures called?

A

mesoderm

bipotenital gonadal ridges (bipotential = not committed to testis or ovaries)

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44
Q

how do testis and ovary development differ?

A

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)

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45
Q

what are the 3 broad causes of early pregnancy loss?

A

errors in embryo foetal development
failure of embryo to implant in uterine lining
inability to sustain development of implanted embryo

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46
Q

define miscarriaage

A

loss of pregnancy prior to 23 weeks gestation
<12 weeks → early clinical pregnancy loss
12-24 weeks → late clinical pregnancy loss

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47
Q

what percentage of conceptions result in preclinical loss? what does this mean?

A

60 percent

preclinical means the pregnancy was undetectable, i.e. before a missed menstrual period

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48
Q

what is the likely major cause of early pregnancy loss?

A

aneuploidy

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49
Q

why does aneuploidy increase with maternal age?

A

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

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50
Q

name 2 cohesin proteins

A

REC8
SMC2
maintain cohesion between chromatids

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51
Q

how is recurrent miscarriage/pregnancy loss defined in the UK?

A

three or more pregnancy losses (consecutive or not)

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52
Q

reduced levels of what might contribute to RPL/RM?

A

LIF in uterine secretions

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53
Q

what aspects do the maternal and paternal genomes contribute to embryo viability?

A

maternal - restrict embryo fitness to conserve resources for future pregnancies
paternal - promote embryo fitness at expense of mother

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54
Q

what are gestational trophoblastic diseases characterised by?

A

overgrowth of trophoblastic tissue

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55
Q

what are the benign causes of gestational trophoblastic diseases?

A

complete and partial hydatidiform moles

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56
Q

what are the malignant causes of gestational trophoblastic diseases?

A

neoplasias (some arising from hydatidiform moles)

  • invasive moles
  • choriocarinoma
  • placental site trophoblastic tumour
  • epithelioid trophoblastic tumour
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57
Q

what is the difference between a complete and partial hydatidiform mole?

A

complete = no fetal tissue present

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58
Q

how does a complete hydatidiform mole arise?

A

empty egg fertilised by two sperm cells or by one sperm cell that’s genome duplicates

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59
Q

how does a partial hydatidiform mole arise?

A

a normal egg is fertilised by two sperm cells or by one sperm cell that’s genome duplicates

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60
Q

what mutations may underly recurrent hydatidiform moles?

A

NLRP7 mutations

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61
Q

what is an ectopic pregnancy?

A

implantation of embryo at site other than uterine endometrium (normally Fallopian tube)

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62
Q

what component of cigarette smoke is thought to contribute to ectopic pregnancy?

A

continine

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63
Q

how is continine thought to contribute to ectopic pregnancy? 2 ways

A

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

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64
Q

how is cannabis thought to cause ectopic pregnancy? 2 ways

A

tHC components may act on the Fallopian tube and perturb embryo transit
OR
alter the endocannabinoid balance in the fT → disrupted embryo environment

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65
Q

what receptors are reduced in ectopic pregnancy patients?

A

cannabinoid receptors CB1

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66
Q

10 risk factors for ectopic pregnancy?

A 
previous ectopic pregnancy
prior ft surgery
STIs
endometriosis
pelvic inflammatory disease
cigarette smoking
cannabis use
≥35 yrs
history of infertility 
IVF
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67
Q

what is the non-selective uterus hypothesis?

A

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

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68
Q

Outline the two types of embryo/foetus nutrition

A

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

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69
Q

what kind of placenta do humans have?

A

haemochorial-type

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70
Q

what’s the function ofnthe connecting stalk?

A

links embryo to chorion

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71
Q

what are trophoblastic lacunae?

A

spaces formed by breakdown of capillaries and uterine glands, filled with maternal blood → intervillous/maternal blood spaces

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72
Q

what are fetal membranes? name them

A

extra-embryonic tissues that forma tough flexible sac encapsulating the foetus
forms basis of maternal-fatal interface
amnion - inner
chorion - outer

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73
Q

what is the amnion?

A

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

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74
Q

when does amniotic fluid start being secreted?

A

from the 5th week

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75
Q

what is the chorion?

A

outer fetal membrane
formed from yolk sac and trophoblast
v vascularized
forms chorionic villi

76
Q

what are chorionic villi?

A

outgrowths of cytotrophoblast from chorion
project through syncitiotrophoblast into maternal endometrium
form basis of fetal side of placenta

77
Q

differences between amnion and chorion

A 
amnion = inner, avascular, epiblast
chorion = outer, highly vascular, yolk sac and trophoblast
78
Q

what is the allantois?

A

yolk sac outgrowth
forms along connecting stalk from embryo to chorion
forms umbilical cord

79
Q

what does the allantois become and how?

A

umbilical cord

becomes coated in mesoderm and vascularises

80
Q

how does the amniotic sac form?

A

the expanding amnion is forced into contact with the chorion and they fuse to form the sac

81
Q

what is the function of chorionic villi?

A

provide surface area for the exchange of gases and nutrients

82
Q

outline the 3 phases of chorionic villi development

A

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

83
Q

explain the terminal villus microstructure and how its suited to function?

A

convuluted knot of vessels and vessel dilation (coated in trophoblast)
→ slows blood flow to allow exchange between maternal and fetal blood

84
Q

how do the terminal chorionic villi change from early to late pregnancy?

A

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

85
Q

outline the succession of maternal blood supply to the endometrium

A

uterine artery → arcuate → radial → basal → spiral (arise during menstrual cycle endometrial thickening)

86
Q

which arteries supply blood to endometrium?

A

spiral arteries

87
Q

outline the process of conversion (i.e. spiral artery remodelling)

A

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

88
Q

how is oxygen transported across the placenta?

A

via diffusional gradient - high maternal oxygen tension and low fetal tension

89
Q

how is glucose transported across the placenta?

A

facilitated diffusion by transporters on maternal side and foetal trophoblast cells

90
Q

how is water transported across the placenta?

A

mostly diffusion

some local hydrostatic gradients

91
Q

how are electrolytes transported across the placenta?

A

diffusion

active co-transport

92
Q

how is calcium transported across the placenta?

A

actively transported via magnesium ATPase calcium pump

93
Q

how are amino acids transported across the placenta?

A

active transport

94
Q

what are some maternal cardiorespiratory changes that occur?

A

increased cardiac output 30%
decreased peripheral resistance 30%
increased blood volume 40%
increased pulmonary ventilation 40%

95
Q

how is foetal oxygen content and saturation similar to maternal blood?

A

even though fetal oxygen tension (partial pressure) is low , fetal Hb has a higher affinity for oxygen than maternal Hb

96
Q

what is the site of gas exchange for the foetus?

A

placenta

97
Q

how do ventricles pump in the foetus? why?

A

parallel instead of series → ↑ efficiency

98
Q

how are the fetal pulmonary and hepatic circulations bypassed?

A

via vascular shunts that close at birth

99
Q

what happens to the fetal respiratory system at ~20weeks?

A

primitive air sacs form and surfactant production begins

vascularisation at ~28weeks

100
Q

what is the theory behind fetal rapid respiratory movements?

A

1-4hr/day during REM sleep

thought to be breathing practice and to develop diaphragm

101
Q

when does the fetal endocrine pancreas start to be functional?

A

from start of 2T , insulin produced from mid-2T

102
Q

what is meconium?

A

first stool passed after birth

formed from digested amniotic fluid containing debris and bile acids

103
Q

when do foetal movements begin?

A

late 1T, detectable by mothers at ~14 weeks

104
Q

from when can the foetus respond to stress?

A

18 weeks

105
Q

when do foetal thallus-cortex connections form?

A

24 weeks

106
Q

what sleep is the foetus mostly in?

A

slow wave or REM

107
Q

How is labour similar to a pro-inflammatory reaction?

A

immune cell infiltration

inflammatory cytokine and prostaglandin secretion

108
Q

what are the 4 phases of parturition?

A

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

109
Q

what are the 3 stages of Labour? (phase 3)

A

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

110
Q

how long are deliveries usually?

A

first - 8-18 hours

subsequent - 5-12 hours

111
Q

what is the function of the cervix? how does its strcuytuee support this?

A

retaining foetus in uterus
high connective tissue content (collagen fibres embedded in proteo-glycan matrix) provide rigidity and stretch resistance

112
Q

how does the cervix remodel throughout pregnancy?

A

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

113
Q

what’s the theory behind the initiation of labour?

A

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

114
Q

what are the functions if CRH in labour?

A

↑ foetal CRH → ↑ ACTH →↑ cortisol
cortisol drives placental production of CRH → ↑ foetal cortisol (positive feedback)
CRH stimulates DHEAS production byu fetal adrenal cortex → oestrogen substrate

115
Q

why is progesterone high during pregnancy?

A

maintains uterine relaxation

116
Q

how do uterine receptors change as term approaches?

A

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

117
Q

what type of hormone is oxytocin and where is synthesized?

A

nonapeptide hormone

utero-placental tissues and pituitary

118
Q

what happens to uterine oxytocin levels at labour onset?

A

sharply increase due to increase in oestrogen levels

release promoted by the Ferguson reflex

119
Q

what is the Ferguson reflex?

A

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

120
Q

through which receptor does oxytocin signal?

A

G-coupled oxytocin receptor OTR/OXTR

121
Q

what inhibits OXTR expression pre-labour? how does this change in labour?

A

progesterone

↑ oestrogen → ↑↑ in uterine oxtr expression

122
Q

what are the functions of oxytocin?

A

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

123
Q

what are the 3 primary prostaglandins secreted in labour?

A

PGE2
PGF2 alpha
PGI2

124
Q

what promotes increased prostaglandin action?

A

↑ estrogen → activates phospholipase A2 enzyme → ↑ arachidonic acid → ↑ PG synthesis
↑ oestrogen → ↑ oxtr expression → ↑ PG release

125
Q

what is the fucntion of PGE2?

A

cervix remodelling

- leukocyte infiltration into cervix, IL-8 release , collagen bundle remodelling

126
Q

what is the fucntion of PGI2?

A

myometrium

- promotes myometriral smooth muscle relaxation and lower uterine segment relaxation

127
Q

what is the fucntion of PGF2 alpha?

A

myometriol contractions

- works w oxytocin to destabilise membrane potentials and promote myocyte connectivity

128
Q

what 2 other factors are involved in cervix remodelling?

A

relaxin

nitric oxide

129
Q

outline myometrial contractions during labour

A

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

130
Q

what happens in the final phase of labour?

A

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

131
Q

why does the uterus remain in a contracted state after delivery?

A

facilitate uterine vessel thrombosis and healing of those vessels and to prevent intrauterine bleeding → uterus restoration and cervix repair

132
Q

why is cervix repair and uterus restoration important?

A

to prevent commensurate bacteria entering uterus

restore endometrial cyclicity in response to hormones to allow implantation of another embryo

133
Q

how is pre-eclampsia diagnosed?

A

new onset hypertension in previously normotensive woman, after 20wks gestation
SBP ≥ 140
OR
DBP ≥90

134
Q

signs and symptoms of pre-eclampsia?

A 
reduced foetal movement
↓ amniotic fluid
oedema
headache
abdo pain
visual disturbances, seizures, breathlessness
135
Q

2 subtypes of preeclampsia? and associated symptoms?

A

early onset - <34wks, fetal and maternal symptoms, changes in placental structure

late onset - ≥34wks , mainly maternal symptoms, fewer placental changes

136
Q

risk factors for preeclampsia?

A 
maternal age ≥40/≤20
family history
autoimmune conditions, diabetes, pcos, renal disease
bmi ≥ 30
previous (gestational) hypertension
137
Q

what are the risks of preeclampsia?

A

damage to maternal kidneys, brain, liver etc
progression to eclampsia - seizures
placental abruption
reduced foetal growth, preterm birth, loss/stillbirth

138
Q

what happens in preeclampsia that differs from normal pregnancy?

A

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

139
Q

what factors does a healthy placenta normally release and their function?

A

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

140
Q

how does a distressed placenta differ in preeclampsia in terms of factors released?

A

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

141
Q

what can be measured to predict PE onset?

A

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

142
Q

what is the only way to resolve preeclampsia?

A

delivery of the placenta

143
Q

managemen options for PE?

A

≤34wks - try maintain pregnancy
≥37wks - delivery preferable
anti-hypertensives
corticosteroids for ≤34 wks to promote lung development

144
Q

how can PE be prevented?

A

weight loss
exercise throughout pregnancy
low dose aspirin for high risk groups

145
Q

what can PE increase the risk of devloping?

A

T2DM
renal disease
CVD
preeclampsia in next pregnancy

146
Q

what factors can affect a foetus that could have a lasting effect?

A

maternal nutrition, illness, stress, medication
fetal infection in utero
environmental exposures

147
Q

what is the barker hypothesis?

A

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)

148
Q

DOHaD proposed mechanism?

A

intrauterine environment leads to epigenetic changes which influence development and physiology

149
Q

what is epigenetic?

A

heritable changes in marks on DNA that dont change nucleotide sequence but influence how genes are expressed

150
Q

outline the NHS healthy child programme?

A

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

151
Q

3 examples of early childhood screening?

A

newborn check
newborn hearing sceren
blood spot check (heel prick test)

152
Q

what are the fundamentals for a good screening test?

A

disease should be identifiable before critical point, treatable and it should prevent / ↓ mortality/morbidity
easy to administer
cost effective
reproducible with accurate results

153
Q

name a programme being used to optimise early life outcomes

A

Sure Start

154
Q

name an NHS screening test undertaken preconception?

A

diabetic eye screening for women with T1DM/T2DM

155
Q

name an NHS screening test undertaken in trimester 1?

A

early scan/blood test for T21, T18 and T13 screening

156
Q

name an NHS screening test undertaken in trimester 2/3?

A

detailed ultrasound for structural abnormalities, T18 and T13
another diabetic eye screen for women with diabetes

157
Q

name an NHS screening test undertaken in a newborn?

A

hearing screen

blood spot screens for SCD, CF, hypothyroidism, inherited metabolic diseases

158
Q

what are the primitive reflexes of gross motor development?

A

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

159
Q

what are the 4 domains of child developmental assessment?

A

fine motor
gross motor
social
speech & language

160
Q

what should be observed in the pull to sit movement?

A

the baby’s head should not lag and it should be able to hold it upright (6/7 months)

161
Q

what are the sitting milestones for babies?

A

6 months - sitting unsupported with round back

8 months - sitting unsupported with straight back

162
Q

what gross motor development should be observed at 6-8wks?

A

raising head to 45º whilst on tummy

163
Q

when should a baby be able to roll over?

A

3-5mths

164
Q

when should a baby start crawling and standing w cruising around furniture?

A

8-9mths

10 mths

165
Q

what are the walking milestones for babies?

A

12 months - unsteady broad gait

15 months - steady walk

166
Q

variations of normal crawling?

A

bottom shuffle
commando crawl
crawling on all 4s

167
Q

what are the vision milestones for babies?

A

6wks - follow moving object by turning head

4 months - reaching out for toys

168
Q

what are the fine motor milestones for babies?

A 
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
169
Q

when should a baby startle to loud noises?

A

newborn

170
Q

when should a baby start vocalising?

A

3-4mnths

171
Q

when should a baby turn to soft sounds?

A

7motnhs

172
Q

when should polysyllabic babble start?

A

7-10months

173
Q

baby language milestones?

A 
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
174
Q

when should a baby start smiling?

A

6 weeks

175
Q

when should a baby be able to feed/drink itself?

A

6-8months using hands
12 months drinking from cup w 2 hands
18 months with holding spoon

176
Q

symbolic play and parallel play age?

A

18-24 mths

2.5-3 years

177
Q

potty trained age?

A

2years

178
Q

what are the patterns of abnormal development?

A

slow but steady
plateau
regression

179
Q

4 main gross motor developments and limit ages ?

A

head control - 4months
sits unsupported - 9 months
stands independent - 12 months
walks independently - 18 months

180
Q

4 main vision and fine motor developments and limit ages ?

A

fixes and follows visually - 3 months
reaches for objects - 6 months
transfers - 9 momnths
pincer grip - 12 months

181
Q

4 main hearing, speech & language developments and limit ages ?

A 
polysyballbi babble - 7 monmths
consonant babble - 10 months
6 words with meaning - 18 months 
joins work - 2 years
3 word sentences - 2.5 years
182
Q

4 main social/emoptional behaviour developments and limit ages ?

A 
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
183
Q

who and when should a baby’s development be monitored?

A

parents, teachers, doctors, nurses
oppurtunistically
as part of the healthy child programme

184
Q

what 4 principles underpin the healthy child programme?

A

screening
immunisation
child health reviews
health promotion

185
Q

what can contribute to a delayed development?

A

ill health
lack of physical/psychological stimuli
seneory/motor impairment
reduced inherent potential

186
Q

types of developmental delay?

A

global eg. downs syndrome, drugs, infections

specific -

  • language eg. hearing loss, autism
  • motor eg. cerebral palsy
  • sensory
  • cognitive

BRS 2 (12 decks)

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