Development and Ageing Flashcards

1
Q

How does placental support for the foetus change throughout pregnancy

A

During first trimester: growth is limited, there is low foetal demand on placenta and the nutrition is histiotrophic: therefore reliant on uterine gland secretions and brakdown of endometrial tissue

2nd trimester onwards: fetal demand increases as switches to haemotrophic support. This happens due to a hameochorial-type placental where materanl blood directly contacts babies chorionic villi.

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2
Q

Describe the different cells involved in the early implantation stage

A

Syncytiotrophoblasts: grow out from the implanted embryo to break down uterine glands, maternal capillaries and endometrial tissue for nutrients
Cytotrophoblasts: proliferative form of syncytiotrophoblasts, important to form chorionic villi

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3
Q

What is chorionic villi

A

Finger like extentions of the chorionic cytotrophoblast

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4
Q

Describe the phases of chorionic villi development

A

Primary: outgrowth of the cytotrophoblast and branching of these extensions (forms villi)
Secondary: foetal mesoderm grows into the primary villi
Tertiary: umbilical artery and vein grow into the villus mesoderm

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5
Q

How does the chorionic villi’s terminal villus microstructure change throughout pregnancy

A

Early pregnancy: 150-200 micrometers diameter, 10 micrometres trophoblast thickness

Late pregancy: villus thinner only 40 micrometres, 1-2 micrometres trophoblast thickness

villi gets thinner and the distance between maternal blood and babies blood decreases

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6
Q

Describe spiral artery remodelling

A

Extra-villus trophoblast (EVT) cells coating the chorionic villi, invade through the decidua and myometrium, down into the maternal spiral arteries, there they becomes known as endovascular EVT cells. EEVT cells activate endothelial cells to release chemokines to recruit immune cells. The immune cell invasion triggers the breakdown of smooth muscle around the vessels and the ECM in the wall of vessels so that EVT coats the inside of the vessels. once inside EVT cells replace the ECM with fibrinoid. This makes the spiral arteries a low pressure and high capacity conduit for blood flow

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7
Q

Describe failed spiral artery conversion

A

Retain smooth muscle so arteries stay spiralled and have contractibility, which affects blood delivery to the IVS
high chance of occlusion
Immune cells surround the wall of unconverted vessel and embed causing an atherosclerotic process, immune cells from plaques- intima hyperplasia

Leads to peturbed/turbulent flow (where goes from thin artery to thick) and local hypoxia, free radical damage and inefficient delivery of substrates from intervillous space

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8
Q

What is the criteria for pre-eclampsia diagnosis

A

New onset hypertension, 140 and above systolic, 90 and above diastolic
After 20 weeks of gestation

Some have:
proteinuria
reduced fetal movement
less amniotic fluid volume
oedema
headache
abdominal pain

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9
Q

What symptoms are associated with severe preeclampsia/ risk of eclampsia

A

visual distrubances, seizures, breathlessness

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10
Q

What are the two subtypes of preeclampsia

A
  • Early Onset: less than 34 weeks, get fetal and maternal symptoms, placental structure chnages, reduced placental perfusion
  • Late Onset: over 34 weeks, maternal symptoms, foetus and placenta are okay
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11
Q

What are the risk factors for preeclampsia

A

previous pregnancy with preeclampsia
BMI over 30
Fx
Over 40 yrs, under 20
Previous hypertension
diabetes, PCOS, autoimmunity
IVF

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12
Q

What risk does preeclampsia pose to
(1) the mother
(2) the foetus

A

1) damage to kidney, liver ,brain, other organs
progression to eclampsia
HELLP syndrome: hemolysis, Elevated liver enzymes, low platelets
placental abruption (placenta separates from endometrium)

2) pre term delivery, reduced fetal growth, fetal death

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13
Q

Describe what placental defects can cause preeclampsia

A

EVT cells only invade to decidual layer as the EVT cells dont switch from proliferative to invasive. Spiral arteries are therefore, not remodelled and placental perfusion restricted as muscle remains in tact and chorionic villi cannot draw enough blood

Placenta makes lots of PLGF, some VEGF, little Flt1.
PLGF (VEGF related) are pro-angiogenic, released into maternal circulation to bind to VEG-F receptors on endothelial cells to make them vasodilate and release anticoagulants.
Flt1 is a soluble receptor for VEGF-like factors , binds to them and limits bioavailability. High Flt-1 reduces pro-angiogenic factors causing endothelial dysfunction. Preeclampsia placentas release sFlt-1, takes up PLGF and VEGF stopping them reaching endotherlial cells

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14
Q

What causes late onset preeclampsia

A

women may have a predisposition to cardiovascular disease, the stress of pregnancy causes it to manifest

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15
Q

What tests are used to predict onset of preeclampsia

A

PLGF: if levels are smaller than 12 its a positive test and highly abnormal, if 12-100 its a positive test and abnormal so inc risk for preterm delivery

sFlt-1/PLGF ratio: is ratio is over 38 then increased risk

tests can only be used week 20-35

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16
Q

What is the management of preeclampsia

A

delivery of placenta
if less than 34 weeks, maintain pregnancy for fetus
is over 37 try to deliver

regular monitoring
anti-hypertensives
magnesium sulphate to prevent seizures
corticosteroids if before 34 weeks to promote babies lung developement

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17
Q

Three ways to prevent preeclampsia

A

Reduce BMI
Exercise throughout pregnancy (is effective even if BMI doesnt change)
Low dose asprin from 11-14 weeks for high risk groups

18
Q

What are the 4 long term risks of preeclampsia

A

risk of CVD
T2D
renal disease
future preeclampsia (esp if early onset)

19
Q

How is Small for Gestational Age defined

A

if fetal weight is under 10th centile (2DS under norm)
Severe SGA if 3rd centile or under

20
Q

What are the three groups of SGA

A

1) small throughout pregnancy but healthy
2) early growth but slows later in third trimester (FGR/IUGR)
3) non-placental growth restriction like infections or genetic issue

21
Q

What is different between SGA and Interuterine Fetal Growth Restriction

A

SGA- fetal neonatal weight, not in-utero growth or physical characteristics at growth

IUGR- clinical definitions of fetuses with signs of malnutrition and in-utero growth restriction regardless of weight percentile

22
Q

What are the two types of IUGR and their characteristics

A

Symmetrical IUGR: earlier in gestation, genetic disorder or infection, reduced cell number but normal cell size, reduced weigh, length and head circumference, poor prognosis, less malnutrition

Asymmetrical IUGR (big head): later in gestation, utero-placental insufficiency, normal cell number but reduced cell size, low weight bu length and head circumference normal, big head and small body, good prognosis, more malnutrition

23
Q

What does IGFR cause

A

Cardiovascular: fetal cardiac hypertrophy, remodelling of fetal vessels
Resp- poor lung maturation,
Neurological- motor defects and cognitive impairments

24
Q

What is the Barker hypothesis

A

DOHaD (developmental origins of health and disease) hypothesis, low birth weight and being small at 2yo who then put on weight rapidly inc risk of coronary events.
Rate of BMI change not BMI at a point in time

25
Q

what is the idea behind DOHaD

A

Maternal malnutrition causes epigenetic changes (marks on DNA that influence gene expression) which influence development and physiology

26
Q

WHat is the NHS healthy child programme

A

prevent disease and promote good health
is universal and to reduce health inequalities

health promotion/obesity prevention
support care giving and care givers
screening
immunisation
identify high risk
signposting

27
Q

Name one screening program used preconception, 1st trimester, as well as one used in 2/3

A

preconception:diabetic eye screening
1st trimester: Bloods for sickle cell and thalassaemia. T21, T18, T13 (combined test). Syphilis, hep B, HIV
2/3: Blood for T21 (quadruple test)
after birth: Newborn hearing screen, blood spot screen for sickle cell, cystic fibrosis

28
Q

Name a programme that uses parent and child education to promote health, for families with children under 5 and on low income

A

Sure Start

29
Q

Describe brain development in an embryo at 4 weeks

A

Prosencephelon, mesencephalon and rhombencephalon make up the future fore, mid and hind brain in order.
pro and mesen is separated by cephalic flexure,
mesen and rhomben by a pontine flexure
the cervical flexure is after rhomben

30
Q

Describe the parts of the brain stem that the foregut, midgut and hindgut develop into at 5 weeks

A

Foregut- telencephalon, diencephalon
Midgut- midbrain
Hindgut- pons, medulla

31
Q

At 8 weeks what parts of the brain develop

A

Foregut develops hemispheres and ventricles
Midgut develops aqueduct
Hindgut develops cerebellum

32
Q

Describe where on white matter would be responsible for extensors, flexors, proximal and distal movements

A

Lateral corticospinal tract: inbetween butterflys top and bottom wing
Anterior corticospinal tract: above and centre of butterflys top winh
Rubrospinal for arm movements to posture/balance and Reticulospinal for movements of posture and locomotion are close to lateral corticospinal tracts
Vestibulospina

33
Q

Describe a reflex arc

A

sensory recptor, to sensory neuron, connects to interneurone which integrates signal and relays sensory impulses to motor neurones, to motor neuron and effector muscle

34
Q

What is developemnt

A

Impression of a child encompassings: growth, further understanding, new skills, more sophisticated response and behaviours
allows for growth of complex skills

35
Q

Describe the median ages and limit ages for gross motor development

A

newborn: limbs flexed, head lag still
6-8 weeks: raise head to 45 degrees when on tummy
6-8 months: sits without support, from round (6m) to straight back (8m)
8-9 months: crawl
10 months: hold onto furniture
12 months: walks unsteadily, broad gait
15 months: walks steadily

SIMPLIFIED:
newborn: flexed posture
7 months: sits without support
1 year: stands independently
15-18 months: walks independently
2 1/2: runs and jumps

LIMIT AGES
head at 45 degrees- 2 months (median 1 1/2)
head control- 4 months
sits with support: 6 months (normal 3)
Sits without support- 9 months (normal 6)
stands independently- 12 months (normal 9)
walks- 18 months (normal 12)

36
Q

Describe the median ages for vision and fine motor development

A

6 weeks: turns head to follow object or face
4 months: reaches out to toys
4-6 months: palmar grasp of objects
7 months: transfer toys from hand to hand
10 months: pincer grip
16-18 months: marks with crayon
18 months: tower of three
2 years: tower of six, can draw a line
3 years : build a bridge, draw circle
3 1/2 years: draw a cross
4 years: build steps, draw a square
5 years: draw triangle

all drawings should be done without seeing it done, if see first then should be able to copy 6 months before expected to draw without

newborn: fixes and follows face
7 months: object from hand to hand
10 months: pincer grip
1 year: points
15-18 months: immature grip of pencil, scribbles
2 1/2: draws

LIMITS
fixes and follows visually- 3 months
reaches for objects - 6 months
tranfers objects: 9 months
pincer grip: 12 months

37
Q

Describe the median ages for hearing, speech and language development

A

newborn: loud noise startles
3-4 months: vocalises alone, coos and laughs
7 months: turns to soft sounds out of sight, makes babbling sounds
10 months: sounds used to name parents
12 months: two to three words other than mama or dada
18 months: shows two parts of body
20-24 months: two or more words to make simple phrases
2 1/2-3 years: talks consistently in 3-4 word sentences

newborn: stills to voice, startles to noise
7 months: turns to voice, polysyllabic babble
1 year: 1-2 words, knows name
15-18 months: 6-10 words, points to four body parts
2 1/2: 3-4 word sentences, understands two joined commands

LIMITS
polysyllabic babble- 7 months
consonant babble: 10 months
6 words with meaning: 18 months
joins words: 2 years
3 word sentences: 2 1/2 years

38
Q

Describe the median ages for social, emotional and behavioural development

A

6 weeks: smiles responsively
6-8 months: puts food in mouth
10-12 months: waves bye, play peekaboo
12 months: drinks from cup with two hands
18 months: hold spoon and gets food to mouth
18-24 months: imaginative play
2 years: can use potty during day, pull off some clothing
2 1/2-3 years: interactive play with others

6 weeks- smiles
7 months: finger feeds, scared of strangers
1 year: cup with two hands and waves bye
15-18 months: feeds with spoon, helps wth dressing
2 1/2: parallel play, clean and dry

LIMITS
smiles- 8 weeks
fear of strangers: 10 months
feeds with spoon: 18 months
symbolic play: 2 - 2 1/2 years
parallel play: 3- 3 1/2 yr

39
Q

What are the three patterns of abnormal development

A

slow but steady
Plateau
Regression

40
Q

What programme is used to asses child development and what three things does it consist of

A

The healthy child programme:
screens
general exams and immunisations
health education and promotion