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Life Support > Week 8 > Flashcards

Week 8 Flashcards

1
Q

How do nutritional demands change in and ex etero? (4)

A

Move from continuous supply to fasting/feeding
Move from glucose/amino acids to fatty diets
Higher metabolic demand
Insulin moves from being dominant hormone to being counteracted

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2
Q

Overview of structure of placenta

A

Basic structural unit is chorionic villus, blood supply through uterine and ovarian arteries

Functions of the placenta include gas exchange, metabolic transfer, hormone secretion, and fetal protection. Nutrient and drug transfer across the placenta are by passive diffusion, facilitated diffusion, active transport, and pinocytosis.

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3
Q

What adaptations occur during third trimester? (5)

A 
Liver efficiency increases (glucose to glycogen)
Free fatty acids formed and stored
Brown fat for perinatal energy
White fat for insulation
Fat stores increase from about 1% to 15%
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4
Q

Where is brown fat stored for perinatal energy? (4)

A

Neck, scapula, sternum, kidneys

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5
Q

What is the role of insulin in fetal life? (4)

A

Increase glucose uptake in muscle, liver and fat
Reduce lipolysis
Reduce amino acid release from muscle
Reduce gluconeogensis / ketogenesis in liver

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6
Q

What hormones prepare the body for breastfeeding during pregnancy? (4)

A

Oestrogen - increase number / size of ducts
Progesterone - increase number of alveoli
Human placental lactogen - alveolar development
Prolactin - prepares for breastfeeding

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7
Q

What prevents lactation pre-birth? When does this stop?

A

Inhibition of prolactin by oestrogen

Oestrogen rapidly falls within 48 hours post-birth

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8
Q

Important component of breast milk

A

Colostrum

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9
Q

What 2 reflexes control breast feeding?

A

prolactin and milk ejection reflex

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10
Q

Describe prolactin reflex

A

Suckling stimulates reflex
Stimulates anterior pituitary to release prolactin, which stimulates alveoli to secrete milk
Inhibited by stress / fear (due to dopamine release by hypothalamus)

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11
Q

Describe milk ejection reflex

A

Initiated by suckling

Mediated by oxytocin (hypothalamus and posterior pituitary)

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12
Q

Benefits of breastfeeding (4)

A

Free
Nutritionally balanced
Immunological support (gastroenteritis, antibodies, reduced rate of pertussis, NEC)
Long term benefits - obesity, allergies, atopic illnesses

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13
Q

Why don’t people breast feed?

A

Maternal choice
Medications
Infections - HIV with high viral load

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14
Q

Potential normal problems with breastfeeding - not pathological (4)

A

PV bleeding in newborn girls
Gynaecomastia - stimulation of breast buds
Small amounts of blood in baby vomit
Mastitis - sometimes requires antibiotics, commonly caused by staph, continue feeding/expressing

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15
Q

How to neonates transition between in / ex utero in terms of nutritional stores?

A

Cope with high rates of hypoglycaemia in first 6 hours (use of fatty acids, ketones, lactate, glycogen)
Conversion of existing fuel supplies

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16
Q

What are the key catabolic hormones during conversion in / ex utero? (4)

A

Adrenaline, cortisol, growth hormone, glucagon

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17
Q

What are the nutritional demands in a neonate? (5)

A 
Brain (65% vs 30% adults)
Growth
Temperature
Basic life maintenance (e.g. breathing)
Infection
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18
Q

What factors can affect feeding in neonate? (6)

A 
Infection
Poor milk supply
Jaundice
Tongue-tie
Cleft lip / palate
Low tone / poor reflexes
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19
Q

What is IUGR? (3)

A

Intra-uterine growth retardation
Low birth weight
Reduced amount of fat
Low levels of reserve for conversion

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20
Q

What are the characteristics of an infant of a diabetic mother?

A 
Macrosomic baby (growth stimulated by insulin)
Neonatal hypoglycaemia (show normalise)
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21
Q

Two examples of inborn errors of metabolism?

A

MCADD - medium chain acyl-CoA dehydrogenase deficiency
Cannot break down fatty acids
Results in hypoglycaemia

Maple syrup urine disease
Unable to break down branch chain amino acids
Leads to build up
Presents with hypoglycaemia and acidosis

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22
Q

What is the purpose of foetal haemoglobin?

A

TO ensure oxygen moves from mother to baby - has higher affinity for oxygen

Babies have less 2,3-DPG

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23
Q

Describe path of foetal blood

Why?

A

Include foramen ovale, ductus arteriosus and ductus venosus

Priortise blood to brain and heart

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24
Q

What keeps ductus arteriosus open in utero? (2)

A

Prostaglandins (by placenta)

Low oxygen concentration

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25
Q

Describe abnormal circulation during transition period

A

Sometimes circulation reverts to foetal circulation (but there is no umbilical cord)

Shunts can remain open

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26
Q

In what conditions does ductus arteriosus remain open (patent)? (5)

A 
Prematurity
Babies with respiratory distress
Down syndrome
Rubella
Congenital heart disease
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27
Q

What happens if ductus arteriosus remains open?

A

Can be asymptomatic OR can cause heart failure

Treat with medications (ibuprofen (reduces prostoglandin) or paracetamol) or surgery

28
Q

Mechanisms of heat loss (4)

A

Convection
Radiation
Evaporation
Conduction

29
Q

Why do babies lose heat so readily?

A

High surface area
Low body fat
Covered in fluid

30
Q

Why do babies have brown fat?

A

To produce heat

31
Q

Why do babies heat so easily?

A

Thin keratin level in skin

32
Q

What are the four phases of lung development?

A

Pseudoglandular (6-17 weeks, branching)
Canalicular (17-26, bronchiole division)
Saccular (27-term, alveolar and capillary development)
Alveolar (term-childhood, Full development)

33
Q

Types of pathology that restrict foetal lung development

A

Extrinsic -
Intrinsic -
Malnutrition
Smoking

34
Q

What is the importance / significance of foetal lung fluid?

A

xxx

35
Q

Lung liquid pathology (3) - with examples

A

Oligohydramnios (early rupture of membranes)
Fetal breathing abnormalities (neuromuscular disorders, phrenic nerve agenesis, CDH)
Delivery without labour (elective caesarean) - can cause transient tachypnoea newborn

36
Q

What is surfactant?

A

Mix of phospholipids, neutral lipids and protein

37
Q

Where is surfanctant produced?

A

In golgi apparatus of type II neumocytes

38
Q

What is the most important surfactant protein?

A

SP-B

39
Q

What support surfactant maturation?

A

Glucocorticoids
Thyroid hormones
Insulin

40
Q

What is hyaline membrane disease?

A

xxx

41
Q

What is the focus of resusciation efforts in neonates?

A

Preventing respiratory arrest (this is much more common than cardiac arrest, which is the main concern in adults)

42
Q

How can you treat apnoea in babies?

A

Caffiene

43
Q

Outline neurological adaptation in issue if there is sustained hypoxia (2 key points)

A

Babies are built to withstand labour
Can uses ketone bodies as energy source, utilise non-oxidative glycolysis
Hypoxia leads to redirection of blood flow in the fetus

44
Q

Factors determining a neonatal emergency

A 
Cardiac arrest
shock
respiratory arrest
cyanosis
recession/tachypnoea
45
Q

Three areas of emergency management strategy of neonates

A

Supportive care
Identification of problem
Treat the treatable

46
Q

Outline supportive care (4)

A

Ventilation
Fluids
Inotropes
Nutrition

47
Q

Outline identification of problem in neonates (3)

A

Cultures
Scans
Blood tests

48
Q

Common potential emergency treatments in neonates (4)

A

Antibiotics
Surgery
Steriods
Immunosuppression

49
Q

Bradycardia in neonates

A

Indicates bigger issue, sign of neonate body trying to prioritise flow to the brain

50
Q

Signs of emergency in neonates

A 
Low heart rate
Pallor
Slow pulse
Apnoea
Gasping 
Recession
51
Q

Using oliguria as measurement in neonates

A

Amount of urine shows potential issues with blood volume (hypovoleamia)

52
Q

What causes sepsis in neonates? 3 routes, potential bugs

A

Congenital
Early onset
Late onset

Group B step (70%)
Listeria
Gram negative organisms

53
Q

Potential treatments for sepsis

A

Penicillin / gentamicin

Cefotaxime / ampicillin

54
Q

Signs of sepsis in neonates

A

Often different from adults - temperature may be LOW, WC may be low, fever, poor feeding, vomiting, pallor, tachypnoea, sleepiness, irritability

55
Q

Management of sepsis - steps

A

Investigate
Resuscitate
Antibiotics
Prepare for consequences (ventilation, fluids, coagulopathy, inotropes)

56
Q

What causes birth asphyxia

A 
IUGR (intrauterine growth restrictiion)
Prematurity
Abnormal CTG (cardio tosograph)
Abnormal fetal blood gas
Difficult delivery
57
Q

Grading birth asphyxia (3)

A

Grade 1 - irritability, poor feeding
Grade 2 - fits, bad feeding, hypertonia
Grade 3 - floppy, intractable seizures, apnoea

58
Q

Describe the window of opportunity to prevent cell death following asphyxia

A

Cells death follows asphyxia by about 24 hours, cooling a baby (early on, 6 hours) with moderate asphyxia can help prevent cell death

59
Q

What are the four components of RDS

A

Weak chest wall
Excess lung liquid
No blood-air approximation
Surfactant deficiency

60
Q

Describe meconium aspiration syndrome

A

Baby aspirates meconium (pre-natal faeces) during birth, which can cause respiratory distress, infection

61
Q

Describe polyhydramnios

A

Can’t swallow fluids

62
Q

Signs of abdominal emergencies

A

Can present with specific or non-specific features - distension, billous vomiting, obvious loops or protrusions

63
Q

Potential causes of abdominal emergencies

A

NEC, malrotation, volvulus, Hirshsprung’s disease

64
Q

Outline the duct dependent heart defects (5)

A

Pulmonary atresia, critical pulmonary stenosis, critical coarctation, transposition of the great arteries, hypoplastic left ventricle

65
Q

Important principles of neonatal ventilation (2)

A

Functional residual capacity - xxx

Minute volume - xxx

66
Q

Relationship between PIP and PEEP

A

PIP-peak inspiratory pressure

PEEP-positive end-expiratory end pressure

Life Support (5 decks)

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