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Semester 4 > Growth > Flashcards

Growth Flashcards

1
Q

how many lobes around nippe

A

20

9/10 are functional - all other are vestigial

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2
Q

what inhibit and promote lactogenesis

A

inhibit

  • oestrogen
  • progesterone
  • dopamine inhibits release of prolactin –> inhibits milk release
  • if milk isn’t released

promote

  • oxytocin (milk ejection)
  • placental lactogen
  • prolactin (milk synthesis)
  • suckling
  • thinking of baby (due to higher areas involved)
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3
Q

what cells contract for milk ejection

A

myoepithelial

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4
Q

what type of cells do prolactin act on in alveoli to increase milk synthesis

A

cuboidal

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5
Q

what hormone is mainly responsible for milk production vs milk ejection

A

production = prolactin from ant. pituitary

release = oxytocin from post. pituitary

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6
Q

name agonists and antagonists for dopamine and their use with breast feeding

A

antagonists to increase lactation (pre-term birth)

  • metacloperamide
  • domperidone

agonists to inhibit (rarely done)

  • bromocriptine
  • cabergoline
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7
Q

5 secretory pathways of milk components

A

1) exocytosis (proteins/ca/phosphate) from ROUGH ER
2) milk fat globules (lipids) from SMOOTH ER
3) immunoglobulin secretion (IgA)
4) osmosis (ions eg. na / k)
5) paracellular route which opens during pregnancy (leads to higher NaCl and lower lactose/K+ in milk)

so v.preterm women will have different breast milk (higher lactose and higher Na+/K+/Cl-)

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8
Q

why is human milk good

A

whey is soluble in acid - soluble in stomach and promotes gastric emptying
(human milk has high whey content)
-whey: lactoferrin/lysozymes/iga

contains lipase =activated with bile salts and helps digestion

LCPUFA = brain and retinal development

immunity
-if delivered at term –> igG via placenta if preterm, igG from breast milk too

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9
Q

lactoferrin

A

inhibits bacterial growth by binding iron - bugs love iron

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10
Q

mother benefits of breast feeding

A

lose weight

relationship with baby

high oxytocin–> uterus contraction—> dec. risk of postpartum haemorrhage

inhibits oestrogen release—> dec. breast cancer/ovarian cancer due to lowered exposure to oestrogen

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11
Q

lung development (5 stages) + GF involved

A
  1. embryonic stage (lung buds from foregut)
    - hepatocyte nuclear factor 3b
  2. pseudoglandular (Branching)
    - Gli protein
  3. canalicular (development of branching)
  4. saccular
    - VEGF for angiogenesis around
  5. alveolar (even as a child developing)

FGF 10, SSH, BMP4 for outgrowth for new end buds

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12
Q

structural pathology of lung

A

before 16 weeks = limits branching (irreversible) –> permanent low alveoli number

after 16 weeks = branching already occurred so only alveoli number and function affected

extrinsic restrictions

  • congenital diaphragmatic hernia
  • effusions
  • thoracic dystrophy/ vertebral abnormalities
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13
Q

lung liquid secretion

A

lung liquid from amniotic fluid

  1. active pumping of CL- into lung (passive movement of Na in)
  2. water follows
  3. positive pressure in lung keeps lung open

lung liquid required for GROWTH not branching therefore important for lung FUNCTION

before birth it is absorbed

  1. active pumping of Na out to membrane cell
  2. out of cell via 3Na/2K
  3. water follows out

during labour, adrenaline stimulates na/k pump
also upon delivery the high O2 will increase Na transport

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14
Q

liquid lung pathologies

A
  • oligohydroamnios (low amniotic fluid–> little/no lung fluid–> lung underdeveloped)
  • neuromuscular tone loss
  • delivery without labour (no adrenaline to increase absorption of liquid)
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15
Q

concentration of ions of lung liquid

A

Na and K is similar to plasma

cl> hco3- > protein

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16
Q

surfactant production control

A

INCREASE

  • activation of their B-adrenergic recptors on type 2 pneumocytes
  • (dexamethasone-glucocorticoids–> stimulate)
  • T4 thyroid hormones

DECREASE

  • insulin decreases maturation of type 2
  • stretch receptors—> -ve feedback
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17
Q

what is key for ensuring spreading of surfactant

A

SPA,B,C –> PG

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18
Q

SPD

A

immune function rather than structural function of surfactant

function = protecting surfactant from external pathogens

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19
Q

what makes up surfactant

A

protein (SP_) + phospholipids + neutral lipids (main bit that dec. surface tension eg. diplamitoyl-phosphatidycholine)

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20
Q

describe surfactant problems with premature birth

A
  • low number of type 2 pneumocytes + alveoli poorly formed
  • later on gestation, pg replaces pi (pg required for spreading of surfactant)
  • SP_ protein decifencies –> further structural problems eg. spreading)
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21
Q

when is a baby considered premature

A

<37 weeks

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22
Q

how is foetal Hb different

A

2 alpha + 2 GAMMA chains

due to change of one AA

means 2,3DPG doesn’t bind as well to deoxy-Hb = high affinity for O2

23
Q

2,3DPG difference between normal and pregnant women

A

normal - binds to deoxy Hb to allow O2 to be released even at high O2 pressures

pregnant - 30% increase so they can release to foetus

24
Q

at birth what happens to the respiratory structures

A

cold temp causes umbilical vessels to constrict

decreases BF to umbilical veins/ ductus venosus(connecting umbilical vein and IVC) –> closure

ductus arteriosus closes due to blow from both sides (increased blood flow in pulmonary artery)

there is a decrease of placental PG to the baby therefore this promotes closure of structures including the ductus arteriosus (pulmonary artery and aoorta)

foramen ovale closes due to the pressure of RA and LA equalising
(o2 causes pulmonary artery to dilate–> dec. resistance–> increased flow –> increased blood returning to L.A–> pressure on both sides of foramen ovale causes it to close)

25
Q

what can be used to treat patent ductus arteriosus

A

NSAIDS to dec. PG = closure

or surgery

26
Q

problems with growth of children(5)

A

faltering growth - WEIGHT crossing down the centiles

short stature - not meeting their height genetic potential

underweight BMI < 2nd gentile for age/gender

overweight BMI > 91st centile for their age/gender

obese BMI > 98the centile for their age/gender

27
Q

what is congenital adrenal hyperplasia

A

usually to do with deficiency of 21-hydroxylase

required to convert progesterone —> deoxy- cortisol/corticosterone production

therefore progesterone —> high androgens (testosterone)

(or it could be 11-beta: deoxy—> cortisol/corticosterone(–>aldosterone)

resulting in low aldosterone–> salt wasting crisis
low cortisol—> hypoglycemia

28
Q

what are the derivatives of the 3 layer embryonic disc

A

ectoderm

  • hair
  • nails
  • skin (epidermis)
  • brain / spinal cord

mesoderm

  • dermis
  • kindey / adrenal
  • vertebrae/ribs from sclerotome
  • heart / blood vessels

endoderm
-lining of digestive and respiratory tracts

29
Q

infant absorption

A
  • stomach is less acidic , WA drugs are easily absorbed (give lower oral dose)
  • less peristalsis—>less gastric emptying (lower dose)
  • less muscle mass/BF to muscles so less intramuscular)
  • skin well hydrated and high SA:weight (low percutaneous)
  • IV = risk of infection
30
Q

infant distribution

A

give higher loading dose

  • high water to lipid ratio (for water-soluble drugs)
  • lower plasma protein binding = high free drug = give lower dose
  • BBB is incomplete in newborns = LOWER dose
31
Q

infant metabolism + paracetamol

A

liver function changes rapidly = unpredictable

paracetamol metabolism –> sulphation (not glucoridation like in adults - phase II)

32
Q

cognitive development

A

piagets
interaction between active child and environment

  • birth to 2yrs = sensorimotor (separate from objects + object permanence)
  • 2yr to 7yrs = pre-operational (egocentric + animistic + conservation of numbers)
  • 7yrs to 12= concrete operational ( can order)
  • 12yrs+ = formal operational (prepositions + testing hypotheses)

new theories - less rigid discrete stages but agrees child is an active learner

33
Q

social development -key milestones

A 
separation anxiety = 9months to 3yrs
first smile = 4 to 6 weeks
fear of dark = 3 to 5 yrs
temper tantrums = 1 to 3yrs
prefers gender specific plays = 4yrs +
34
Q

social development theories

A

bowlby = monotropy for first 2 yrs

harlows = taken baby monkeys from mother to wired/cloth ‘mothers’

  • proved bowlby wrong (monotropy/2yrs)
  • importance of nurture due to to more to the cloth

rutler = quality vs loss (boys who lost due to illness/death = less crime vs those who due to stress/psychological)
-proves its not the separation itself causing crime

ainsworth/bell = strange situation
-secure (when mother returned they were ok with stranger)
-insecure avoidant
-insecure resistant
attachment type depends on bond with caregiver+ how sensitive to Childs needs

35
Q

language milestones

A 
babbles = 4 to 6months
1st word = 10-12months
10 words = 18 months 
someone else from family understands you = 3yrs
sentences = 2-3yrs
fluently + grammar = 5yrs+
36
Q

language theories

A

behaviourists = reward for imitating

Chomsky = innate ability to learn language needing only exposure to language

Piaget = reflection of thought (language did not contribute to thought)

vygotsky = (language + thought interaction)

intentionality = interactions generated by child promote language learning

37
Q

moral development

A

piagets

  • preschool = damage done
  • older = intention vs mistake
  • older = considering wider social issues

l. kohlberg (6 stages with 3 levels)
- preconventional morality
- conventional morality
- post-conventional morality

38
Q

family life cycle

A

succesful transitioning from each stage to next = good relationships/ prevent disease and emotional stress

  1. independence stage
  2. coupling
  3. parenting
  4. empty nest
  5. retirement / senior stage
39
Q

surfactant production

A

1) precursors enter type II
2) surfactant produced in ER
3) stored in lamellar bodies inside type II
4) lamellar bodies are secreted and form into TUBULAR MYELIN lining the inside of alveolus

Tubular myelin will be degraded by macrophages and recycled

turnover of surfactant every 10hrs

40
Q

foetus circulation

+ what is umbilical artery a branch of

A

umbilical artery–> umbilical vein–> towards liver–> ductus venosus–> IVC (mixed oxygenated/de-oxygenated)–>right atrium–> foramen ovale/if up pulmonary artery - ductus arteriosus—> aorta

umbilical artery is a branch of internal iliac arteries

41
Q

growth charts:

  • what centiles are expressed
  • how many SD does each line represent
A

0.4th to 99.6th

2/3 SDs

42
Q

how does breast milk change during a feed/ over post partum

A

over post partum

  • increase in lactose
  • decreasing of salt Na+/Cl-/K+

over a feed
-increase in fat (hind milk)
therefore important for baby to empty the breast

43
Q

why is whey better than casein

A

more soluble in acid so is more soluble in stomach and promotes gastric emptying

44
Q

what conditions can breast milk prevent vs formula

A

contains LCPUFA = brain and retinal development

prevents necrotizing enterocolitis (NEC)

45
Q

When does surfactant production begin

A

week 25

46
Q

what in surfactant reduces surfaces tension

A 
dipalmitoyl phosphatidylcholine  (DPPC)
(disaturated)
47
Q

factors that are important in the maturation of surfactant during uterine life.

A

glucocorticoids
(eg. dexamethasone) act on B2 of pnuemocytes INCREASING DPPC/surfactant

T4/TRH increases

insulin INHIBITS
-production of surfactant
-production of PG (spreading)
therefore if mother is diabetic–> high glucose in foetus–> production of insulin—> resp distress

48
Q

4 surfactant proteins

A

SPA
-structure of tubular myelin

SPB

  • formation of tubular myelin
  • deficiency leads to low PG

SPC

  • absorption and spreading of the phospholipids
  • deficiency often in interstitial lung disease

SPD
-immunological function

49
Q

what organ produces the chains of foetus’ Hb chains

A
  1. yolk sac
  2. liver- gamma
  3. spleen - gamma + little beta
  4. bone marrow - beta
50
Q

Patent Ductus Arteriosus - why does it lead to breathing problems

A

oxygenated blood that has just entered into the aorta (where pressure is higher) from the LV flowing back into the pulmonary artery and going to the lungs

this increased blood to lungs–> increases the pressure in the lungs making them harder to inflate.

51
Q

why are preterm babies skinny

A

start to produce insulin in 3rd trimester to lay down fat stores - misses out

52
Q

causes of neonatal hypoglycaemia examples

A

Glycogen storage disease (type 1) - no glucose - 6 phosphatase (cant turn g6p–> glucose)

Galactosaemia
cant break down lactose to galactose(in lactose) –> glucose
(missing galactose-1-phosphate uridyl transferase)

53
Q

after how many months does the baby start to make its own igGs

A

3 months

54
Q

what vaccine CAN be given at birth

A

BCG (for high TB risk new borns only)

Semester 4 (10 decks)

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