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s4 - Repro, Develop, Ageing, Pharm > DEVELOP - SYSTEMS > Flashcards

DEVELOP - SYSTEMS Flashcards

1
Q 
What are the 5 stages in respiratory development?
3-8wks
5-16wks
16-26wks
24wks-term
36wks to 5yrs
A 
Embryonic
Pseudoglandular 
Canalicular
Saccular
Alveolar
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2
Q

In which stages of respiratory development does the blood-gas barrier thin and the surfactant system maturation begin?

A

Canalicular and saccular stages

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3
Q

At birth 1/2 the number of alveoli are present, when do we have them all

A

by 5yrs

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4
Q

Branching of bronchi forms bronchioles and terminal bronchioles. Each bronchiole divides to form 2+……which divide into 3-6…….which delvelop…..

A

Bronchiole –> form 2+.. RESPIRATORY BRONCHIOLES which divide into 3-6 ALVEOLAR DUCTS which delvelop TERMINAL SACS

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5
Q

Forkhead TFs (FOXA1/2) factors is involved in proliferation, branching and differentiation of the developing airway. Name 2 other growth factors required:

A
  • Fibroblast GF-10, Sonic Hedgehog, bone morphic protein 4
  • GH
  • VEGF (vascular endo. GF) for angiogensis round alveoli
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6
Q

Saccules develop with capillaries around them at 24wks under which GF?
When do shallow indentations appear in the alveoli?

A

VEGF

32wks

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7
Q

Type I and Type II pneumocytes are present from 22wks. From 24wks what arise? What do they do?

A

Lamellar bodies in Type II pneumocytes

Fuse with cell membrane and release surfactant into extracellular space

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8
Q

Suggest 3 abnormalities that may affect resp development via extrinsic restriction of the lungs:

A
  • CDH so thoracic contents pushed up
  • effusions around lung
  • thoracic/vertebral abnormalityies
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9
Q

Suggest 2 abnormalities that may affect resp development intrinsically:

A
  • lung cysts (cystic adenomatoid malformation)
  • malnutrition e.g. vit A deficient reduces septation
  • smoking reduces foetal lung volumes
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10
Q

At mid-gestation foetal lungs make 5ml/kg fluid..at term 20ml/kg. How do the fluid composition of Cl and HCO3- compare to that of plasma?

A

-higher Cl-, lower HCO3-, lower protein

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11
Q

Lung fluid is produced by actively pumping which ion form the interstitium to the lung lumen? Result?

A

Cl-
Na+ moves passively into lumen, H20 follows by osmosis
Results in a positive pressure in the lung (1cm H20) and this distention keeps the lungs open

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12
Q

To adapt to survive extra-uterine life, the lung fluid must be absorped before birth. How is this done? Via active pumping of …..into the cell from the lumen..

A

Na+ into cell then secreted into interstitium by Na/K ATPase. Cl- and H20 flow passively to interstitium.

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13
Q

What stimulates the absorption of lung fluid in labour? Before the 02 exposure exaggerates reabsorption…(Name 3 hormones)

A

In labour, adrenaline stimulates the Na+ transporters.

THs and cortisol are needed for maturation of the foetal lung response to adrenaline.

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14
Q

What effect can oligohydramnios have on the lung development?

A
  • fluid is pushed out the lungs, they are hypoplastic/underdeveloped
  • vasculature develops abnormally
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15
Q

What is TTN when does it occur (resp)?

A

Transient Tachyponea of the Newborn

-in C-section, baby doesnt get signal to absorb lung fluid (steroids/adren.) so pumps not activated

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16
Q

What is the main component of surfactant made in the endoplasmic reticulum?

A

PC-Phosphatidycholine

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17
Q

Surfactant is made in what cell? Stored where? Released then degraded where? Absorbed and how much is recycled? Turnover time is 10hrs

A

Made in Type II pneumocytes
Stored in Lamellar bodies
Degraded in alveoli
90% recycled

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18
Q

What type of receptors regulate release via negative feedback?

A

Stretch receptors, B adrenergic

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19
Q

What is the function of surfactant? 3 things

A 
Decrease surface tension so alveoli dont collapse
Prevents atelectasis (incomplete inflation)
Reduces work of breath
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20
Q

At 37degrees what organised structure does surfactant form compared to when complressed into a gel and a certain phase with a surface tension of O?

A

37: forms organized tubular myelin
Compressed: from gel to a liquid crystal phase

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21
Q

Surfactant is a mix of phospholipids, neutral lipids and protein. 80% is phosphatidylcholine of which 60% is in what form? What does this do?

A

Disaturated at DPPC (dipalmitoyl phosphatidylcholine)

This is what decreases surface tension and promotes the spreading of surfactant through lungs

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22
Q

10% surfactant by mass is made up of proteins Sp-A,, B C & D. Sp-A is a large glycoprotein. On what gene is it expressed? When is production high? What does it do?

A
  • chromosome 10 (only expressed in lung)
  • production increases lots after week 28
  • determines tubular myelin structure, immunity, spreading of phospholipids..
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23
Q

Sp-B makes up 2% of surfactnat is coded by gene on chromosome 2. What increases its expression and what is it needed for?

A

Increased by glucocorticoids

Needed for tubular myelin, spreading, increases lung compliance and protects surfactant

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24
Q

What does Sp-C (chrs 8, 35a.acids long) enhance? As well as the spreading of phospholipids.

A

Absorption of surfactant

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25
Q

Sp-D has no structural function, what does it do?

A

Immune protection from ext pathogens, expression increases with gestation

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26
Q

What is produced more at the end of gestation and increases the % of DPPC?

A

Glucocorticoids

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27
Q

TRH increases phospholipid independent of T3/4.

T3 crosses the placenta. What effect does T4 have on surfactant production?

A

Increases production

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28
Q

What effect does insulin have on the maturation of type II pneumocytes and the amount of DPPC? Hence effect of diabetes to baby’s lungs?

A

Insulin delays maturation, and decreases amount of DPPC.

So diabetes, hyperinsulinism –> delayed lung maturation

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29
Q

What surfactant pathology may arise with prematurity? PC? capillary membrane?

A

PC less saturated, unstable, buckles on expiration

Leaky cap. membranes->fibrin deposition->inhibits reduction of s.tension, less gas diffusion

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30
Q

What surfactant pathology may arise with no Sp-B?

A

Less PG no secretion of normal surfactant. Lethal

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31
Q

Interstitial lung disease may present with a deficiency in which Sp protein?

A

Sp-C deficiency

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32
Q

In labour liquid production stops, foetal breathing stops. What stimulates breath? What detects hypoxia? Where is the fluid absorbed?

A
  • cooling stimulates breath
  • central chemoreceptor detects hypoxia
  • some fluid squeezed out, most absorbed into lymphatics and capillaries
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33
Q

What 3 areas in the ventrolateral brainstem regulate breathing?

A

VRG (ventral resp. group)
DRG
Pneumotaxic areas

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34
Q

Normal breathing rhythm is active inspiration and passive expiration. As adults become hypoxic they breathe harder and faster, what about in utero foetus? Premature?

A

Opposite, efforts decrease until almost not breathing

Premature baby’s respond like foetus (apnoea)

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35
Q

V. premature baby’s after labour may respond to the hypoxia like a foetus, apnoea. What is given pos-delivery to prevent this?

A

Caffeine. Improves breathing, decreases hypoxia, avoids apnonea

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36
Q

What do baby’s utlise for energy to the vital organs throughout labour with is to a degree hypoxic?

A

Anaerobic glycolysis

Ketone bodies

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37
Q

Surfactant forms a tubular myelin network that live the alveolus keeping it open. What cell degrades it and what is re-used?

A
  • Macrophage
  • phospholipids reused in type II cell
  • some choline fatty acids are lost
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38
Q

Why is the immune response in early life dampened vs. adult?

A
  • immunosuppressive environment of the womb

- regulated immune responses to avoid inflamm. response to benign antigens

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39
Q

Give 3 consequences of the decreased immune response in newborns:

A
  • more susceptible to pathogens e.g. group B strepto.
  • reduced vaccine response
  • may influence asthma/allergy development
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40
Q

Non-antigen specific immunity you are born with. What is antigen specific immunity?

A
  • responds to specific antigens, potentiates response
  • commits to memory for enhanced subsequent response
  • B and T lymphocytes
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41
Q

What do infants recognise pathogens by that they have receptors for on leukocytes e.g. TLR?

A

PAMPs - Pathogen Associated Molecular Patterns (these are highly conseverd and are required for pathogen to function)

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42
Q

Name the 2 primary lymphoid organs:

A
  • Thymus

- Bone Marrow

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43
Q

Suggest 3 secondary lymphoid organs:

A
  • spleen
  • lymph nodes
  • tonsils, adenoids
  • mesenteric meyers patch
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44
Q

The mesoblastic stage of immune development is predominately morphologically recognised what cells in the yolk sac? From 18days gestation, persists for how many weeks?

A

Haematopoetic cells

Persists for 10 weeks

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45
Q

What 3 stages of immune development follow the Mesoblastic stage for site of blood production:

  • 6-8th week
  • 7-9th week
  • 10th-birth
A

Hepatic
Splenic
Myeloid/Bone Marrow

46
Q

Infants having more of which inteleukin makes them have heightened stimulation of Treg. cells?

A

IL-6

47
Q

T cells migrate from the bone marrow to thymus for gene rearrangements and maturation. Then what happens?

A
  • each has a unique antigen receptor on cell surface

- mature T cells exit, re-circulate 2dry lymphoid organs

48
Q

Do T cells cross the placenta?

A

No

49
Q

From which pharyngeal pouch does the Thymus develop?

A

3rd

50
Q

Why is there a trough in IgG levels 3 months after birth?

A
  • newborns are deficient in their own generated IgG
  • have transplacental maternal IgG
  • maternal IgG half life is 1 month
51
Q

When are full adult levels of IgG reached?

A

4-5yrs

52
Q

Infants have higher plasma neutrophils but are less effective. Give 3 reasons why:

A
  • dont migrate to sites of infection
  • poor phagocytosis
  • less efficient bacteriocidal activity
  • dont adhere well
  • express less co-stimulatory molecules (less activation)
53
Q

Neonates have “developmental immunodeficiency” what does this mean? Why is this the case?

A
  • reduced quality &function of immune response and physiochemical barriers
  • to shape dynamically to the demands of early life and adapt appropriately
54
Q

Neonates have increased susceptibility to infections, suggest 1 common bacterial and 1 common viral infection and why they get it more.

A
  • Group B streptococcus (Ig and complement deficient, less phagocytic cells at infection)
  • Herpes Simplex (Ig, cytokine, MO and NK deficiency and less cytotoxicity of T cells)
55
Q

State 3 components of breast milk and their function.

A

Complement for opsonisation
Lysozyme attacks bacterial cell wall
Lactoperoxidase is antistreptococcal
Lactoferrin inhibits bacteria growth

56
Q

Why are IUGR baby’s especially immunocompromised?

A

Smaller Thymus

Poorer T cell function, less T cells as less proliferation

57
Q

BCG vaccine is given at birth, from 2months name 3 vaccines given.

A
  • DTaP (diptheria, tetanus, pertussis, haemophilus influenza)
  • Type B Polio
  • Streptococcus pneumoniae
  • Nisseria Meningitis
58
Q

What effect would maternal vaccination during pregnancy have on immune response? Why?

A

Better, antibodies increase, cross placenta providing specific protection for first few months of high risk life (before vaccine administered)

59
Q

Adult Hb has 4pp chains. 2a, 2beta, what about foetal Hb? Where is foetal Hb synthesised before wk 6, after, and before birth?

A
  • 2a, 2γ chains
  • yolk sac makes it up to 6wks gestation
  • from 6wks liver takes over
  • before birth spleen takes over
60
Q

Foetal Hb is made up of 2a, 2γ chains, how does this change at birth? And what after birth does synthesis?

A
  • at birth beta shoots up and γ plummets

- bone marrow takes over synthesis (2a, 2b)

61
Q

Which way is O2-dissociation curve shifted in the foetus? Why?

A

Left

-increased O2 affinity so binds it at lower partial pressures/ is “stickier”

62
Q

What binds to deoxygenated Hb in adults, that shifts O2-dissociation curve to the right? What happens to this in pregnancy?

A

2,3 DPG - promotes further O2 release and makes it harder for O2 to bind
-30% increase in 2,3 DPG in pregnancy

63
Q

The umbilical vein travels towards the liver, ~55% of foetal blood bypasses the hepatic vessels via what vessel? That shunts the blood where? Where does the rest go?

A
  • The ductus venosus shunts this blood to IVC

- Rest will enter the portal vein

64
Q

The blood in the RA of foetus is mixed as the deoxygenated blood from the legs in the IVC is combined with what?

A

The oxygenated blood from the umbliical vein

65
Q

Most foetal blood in the RA is shunted through where?

A

The foramen ovale into LA

66
Q

Give 3 reasons blood is unlikely to enter lungs in the foetus.

A

-lungs are fluid filled
-lung capillaries are v.constricted -> high pressure&resistance
~no blood enters RV (RA–>LA)
-if does, will be shunted via ductus arteriosus -> aorta

67
Q

The umbilical artery where some blood goes to placenta for CO2/waste removal and oxygenation is a branch of which vessel?

A

The internal iliac

68
Q

At birth what causes the umbilical vessels to constrict? As a result what closes after 3-10days?

A
  • cooler temps after cord is clamped

- d.venosus closes as blood no longer flows in umbilical vein

69
Q

Upon birth and air breathed, fluid is pushed out lungs. What causes the pulmonary arterioles to dilate reducing resistance? What closes in minutes-hrs of birth? How?

A
  • O2 causes the v.dilation
  • less pulmonary resistance, RA and RV at lower pressure as more blood returns to LA
  • RA/LA pressures equalise
  • foramen ovale closes
70
Q

What 2 things cause the ductus arteriosus to close in 96hrs?

A
  • O2 rise

- prostoglandin decrease as placenta gone

71
Q

Abnormal circulation or reversion to foetal anatomy can occur. Esp as the pulmonary arteries are v. reactive. Suggest 2 causes of them constricting?

A
  • hypoxia
  • hypercarbia
  • acidosis
  • cold
  • -> rise in PVR causing L->R shunting
72
Q

PDA (patent d. arteriosus) can increase the work of breathing and lead to congestive HF by 1yr. List 3 symptoms:

A
  • fast breathing
  • sweating during feeding, poor feeding
  • poor growth
  • rapid pulse, bounding pulse
73
Q

PDA (patent d. arteriosus) can increase the work of breathing, how?

A
  • the defect causes increased blood to enter the lungs
  • pressure in the lungs is greater
  • harder to inflate
74
Q

Give 3 groups that the defect PDA (patent d. arteriosus) is common in.

A
  • premature
  • resp. distress due to hypoxia
  • Down’s S.
  • Rubella
  • Congenital HD
75
Q

PDA (patent d. arteriosus) is treated by which NSAID? How does this help? (Or surgery to ligate)

A

-Indomethacin: inhibits prostoglandins so encourages closure

76
Q

What kind of shunting does an ASD (atrial septal defect) cause?

A

-acyanotic L–>R due to high compliance of RA and change in pressure across the 2 atria

77
Q

Give 3 symptoms of an ASD (atrial septal defect).

A
  • dysponea
  • frequent resp. infections
  • palpitations
  • SOB on activity
78
Q

Give 2 reasons why neonates are at risk of heat loss.

A
  • high SA:body mass
  • lower % body fat, less subcut fat
  • cannot shiver
79
Q

How do babies do non-shivering thermogenesis?

A

-brown fat mitochondria with uncoupled movement of H+ to ATP, instead makes heat via uncoupling protein

80
Q

Babies brown fat non-shivering thermogenesis is controlled by what innervation?

A

Sympathetic innervation of brown fat

Highly vascularised to warm blood

81
Q

Why is it important to dry the baby after birth?

A
  • hypothermia is a major cause of neonatal death

- heat can be lost from wet skin by evaporation

82
Q

Neonates have a v.high total body water that decreases with age. Before vs after birth where is the water distributed?

A
  • most extracellular before
  • near birth this decreases and more into ICFV
  • at 6months ICFV>ECFV
83
Q

Fluid in the neonate is lost from kidneys, stool, the resp tract (humidity and temp. dependent)…where else that particularly impacts premature babies?

A

-the skin as skin isnt fully developed in preterms

84
Q

Completion of nephrons occurs at 34wks but they are immature at birth so how is GFR vs adult?

A

GFR is reduced in neonates

85
Q

What about the renal tubules concentrating ability of a neonate?

A

Limited concentrating ability as transporters not at optimum function to transport Na+ and gluc. from tubule to blood to make a conc grad for H20 re-absorption in interstitial space

86
Q

What is the definition of intelligence?

A

-persons cognitive ability to learn

87
Q

Suggest 4 things intelligence is associated with:

A
  • school performance
  • IQ, logic
  • abstract thought
  • emotional knowledge
  • memory, planning, creativity
88
Q

Intelligence has 2 important feautures, what are they?

A
  • capacity to learn from experience

- ability to adapt to environment

89
Q

Intellegence is seen as a broad, underlying category, “g” then multiple specialist skills e.g. visuospatial..why is intellegence hard to define/test?

A

-poor learners find test hard, good learners find tests easier and perform better

90
Q

What does Jean Pinget’s Model of Cognitive development say about how a child functions and develops modes of thought?

A
  • child is like scientist solving problems
  • development progresses as child manipulates its environment
  • actively works to develop more rational/logical modes of thought
91
Q

According to Jean Pinget’s Model of Cognitive development, what are “operations”?

A
  • via environment interaction, child forms a set of internal cognitive rules that allow child to make sense of the world.
  • these are operations
92
Q

According to Jean Pinget’s Model of Cognitive development, “operations”, what happens if the event is in disequilibrium with thought? 2 processes

A
  • Assimilation: modifies percieved environment to fit existing knowledge structure
  • Accomodation: modifies knowledge to fit new environmental challenge
93
Q

Give an example of assimilation and accomodation to disequelibrium when a child knows “4legs+tail=dog”…

A

Assimilation - 4 legs+tail+bark = dog

Accomodation - 4 legs+tail + meow = cat

94
Q

What are schemas?

A

-internalised representations of generalised classes of actions/situations

95
Q 
Jean Pinget's Model of Cognitive development has 4 stages, what are they?
Birth-2yrs
2-7
7-12
12+
A

Birth-2yrs: SENSORIMOTOR
2-7: PREOPERATIONAL
7-12: CONCRETE OPERATIONAL
12+: FORMAL OPERATIONAL

96
Q

What does the Sensorimotor stage of Jean Pinget’s Model of Cognitive development say about how you act and develop?

A
  • realise your separate from objects and are an agent of action so begin to act intentionally
  • develop “object permanence” (Aware object still exists if hidden)
97
Q

What does the Preoperational stage of Jean Pinget’s Model of Cognitive development say about how you learn, think and develop?

A
  • learn to use language
  • egocentric and animistic thinking
  • conservation of numbers
98
Q

What does the Concrete Operational stage of Jean Pinget’s Model of Cognitive development say about how you develop?

A
  • think logically about objects/events
  • conservation of mass and weight
  • can order objects in series/categories
99
Q

What does the Formal operational stage of Jean Pinget’s Model of Cognitive development say about how you think/develop?

A
  • think logically about abstract prepositions and test hypothesises systematically
  • can consider the hypothetical, future and ideology
100
Q

Separation anxiety begins at 9months to 3yrs, when does it peak?

A

18months

101
Q

What does “The Bolby Theory of Attachment” say about attachment an social releasers driving care?

A
  • children are pre-programmed to form attachments to survive

- social releasers e.g. cry/smile are innate behaviours to keep care giver close. These are instinctive

102
Q

What did Rutter have to say about the effect of loss/disruption of care on children?
e.g. maternal deprivation due to cancer…vs arguements…child more likely -> crime

A
  • its the quality of the relationship lost

- its the conflict/stress before the separation that causes antisocial behaviour

103
Q

“The Bolby Theory of Attachment” says Attachments can be secure or insecure. And forms a template for our future relationships. Name the 4 characteristics of attachment:

A
  • Safe Haven
  • Secure Base
  • Proximity Maintenance
  • Separation Distress
104
Q

Only long alleles on the 5-HTTLPR gene is v likely to lead to secure attachments in development. What about 2 short alleles on this gene?

A
  • only secure if care is sensitively responsive

- otherwise insecure attachments will form

105
Q

What is meant by a child’s “temperment”?

A
  • style of behaviour/”how” of behaviour

- biological, born with

106
Q

What are the 3 aspects of temperment?

A
  • emotionality
  • activity
  • sociability
107
Q

Kohlberg argued we develop from
-a selfish desire to avoid punishment…..
-to concern for group functioning…
-to concern for consistent application of universal ethical principles.
What do each of these represent?

A

Personal
Societal
Morality

108
Q

Erikson’s theory of development aka Crisis resolution is based on what?

A
  • stages in early life

- each stage has own dilemmas, you remain in the stage until you adapt to that

109
Q

Morality development begins with pre-conventional morality in primary school to conventional morality is society, what do these represent? NB: post-conventional morality is an ideal

A
  • pre-conventional: punishment and obedience, reward, what is fair
  • conventional: be good for approval, uphold laws and societal rules
110
Q

Family life cycle says we pass through distinct stages from crib-coffin and must master the skills of each stage to move on, give an adv of smooth transitions and a disadv of not mastering skills?

A
  • adv: less disease, and emotional/stress-related disorder

- disadv: more likely to have difficulty with relationships and future transitions

111
Q

What are the 5 stages in the Family Life Cycle model

A
  • idependence
  • coupling
  • parenting children
  • empty nest
  • senior
112
Q

Parenting can be authoritative, authoritarian or permissive, what makes up the best parenting?

A
  • authoritative (firm boundaries but nuturing)
  • flexible boundaries that fit childs emotional needs
  • attachment with child will form the template for their future relationships

s4 - Repro, Develop, Ageing, Pharm (14 decks)

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