Week 8 Flashcards
How do nutritional demands change in and ex etero? (4)
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
Overview of structure of placenta
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.
What adaptations occur during third trimester? (5)
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%
Where is brown fat stored for perinatal energy? (4)
Neck, scapula, sternum, kidneys
What is the role of insulin in fetal life? (4)
Increase glucose uptake in muscle, liver and fat
Reduce lipolysis
Reduce amino acid release from muscle
Reduce gluconeogensis / ketogenesis in liver
What hormones prepare the body for breastfeeding during pregnancy? (4)
Oestrogen - increase number / size of ducts
Progesterone - increase number of alveoli
Human placental lactogen - alveolar development
Prolactin - prepares for breastfeeding
What prevents lactation pre-birth? When does this stop?
Inhibition of prolactin by oestrogen
Oestrogen rapidly falls within 48 hours post-birth
Important component of breast milk
Colostrum
What 2 reflexes control breast feeding?
prolactin and milk ejection reflex
Describe prolactin reflex
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)
Describe milk ejection reflex
Initiated by suckling
Mediated by oxytocin (hypothalamus and posterior pituitary)
Benefits of breastfeeding (4)
Free
Nutritionally balanced
Immunological support (gastroenteritis, antibodies, reduced rate of pertussis, NEC)
Long term benefits - obesity, allergies, atopic illnesses
Why don’t people breast feed?
Maternal choice
Medications
Infections - HIV with high viral load
Potential normal problems with breastfeeding - not pathological (4)
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
How to neonates transition between in / ex utero in terms of nutritional stores?
Cope with high rates of hypoglycaemia in first 6 hours (use of fatty acids, ketones, lactate, glycogen)
Conversion of existing fuel supplies
What are the key catabolic hormones during conversion in / ex utero? (4)
Adrenaline, cortisol, growth hormone, glucagon
What are the nutritional demands in a neonate? (5)
Brain (65% vs 30% adults) Growth Temperature Basic life maintenance (e.g. breathing) Infection
What factors can affect feeding in neonate? (6)
Infection Poor milk supply Jaundice Tongue-tie Cleft lip / palate Low tone / poor reflexes
What is IUGR? (3)
Intra-uterine growth retardation
Low birth weight
Reduced amount of fat
Low levels of reserve for conversion
What are the characteristics of an infant of a diabetic mother?
Macrosomic baby (growth stimulated by insulin) Neonatal hypoglycaemia (show normalise)
Two examples of inborn errors of metabolism?
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
What is the purpose of foetal haemoglobin?
TO ensure oxygen moves from mother to baby - has higher affinity for oxygen
Babies have less 2,3-DPG
Describe path of foetal blood
Why?
Include foramen ovale, ductus arteriosus and ductus venosus
Priortise blood to brain and heart
What keeps ductus arteriosus open in utero? (2)
Prostaglandins (by placenta)
Low oxygen concentration
Describe abnormal circulation during transition period
Sometimes circulation reverts to foetal circulation (but there is no umbilical cord)
Shunts can remain open
In what conditions does ductus arteriosus remain open (patent)? (5)
Prematurity Babies with respiratory distress Down syndrome Rubella Congenital heart disease
What happens if ductus arteriosus remains open?
Can be asymptomatic OR can cause heart failure
Treat with medications (ibuprofen (reduces prostoglandin) or paracetamol) or surgery
Mechanisms of heat loss (4)
Convection
Radiation
Evaporation
Conduction
Why do babies lose heat so readily?
High surface area
Low body fat
Covered in fluid
Why do babies have brown fat?
To produce heat
Why do babies heat so easily?
Thin keratin level in skin
What are the four phases of lung development?
Pseudoglandular (6-17 weeks, branching)
Canalicular (17-26, bronchiole division)
Saccular (27-term, alveolar and capillary development)
Alveolar (term-childhood, Full development)
Types of pathology that restrict foetal lung development
Extrinsic -
Intrinsic -
Malnutrition
Smoking
What is the importance / significance of foetal lung fluid?
xxx
Lung liquid pathology (3) - with examples
Oligohydramnios (early rupture of membranes)
Fetal breathing abnormalities (neuromuscular disorders, phrenic nerve agenesis, CDH)
Delivery without labour (elective caesarean) - can cause transient tachypnoea newborn
What is surfactant?
Mix of phospholipids, neutral lipids and protein
Where is surfanctant produced?
In golgi apparatus of type II neumocytes
What is the most important surfactant protein?
SP-B
What support surfactant maturation?
Glucocorticoids
Thyroid hormones
Insulin
What is hyaline membrane disease?
xxx
What is the focus of resusciation efforts in neonates?
Preventing respiratory arrest (this is much more common than cardiac arrest, which is the main concern in adults)
How can you treat apnoea in babies?
Caffiene
Outline neurological adaptation in issue if there is sustained hypoxia (2 key points)
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
Factors determining a neonatal emergency
Cardiac arrest shock respiratory arrest cyanosis recession/tachypnoea
Three areas of emergency management strategy of neonates
Supportive care
Identification of problem
Treat the treatable
Outline supportive care (4)
Ventilation
Fluids
Inotropes
Nutrition
Outline identification of problem in neonates (3)
Cultures
Scans
Blood tests
Common potential emergency treatments in neonates (4)
Antibiotics
Surgery
Steriods
Immunosuppression
Bradycardia in neonates
Indicates bigger issue, sign of neonate body trying to prioritise flow to the brain
Signs of emergency in neonates
Low heart rate Pallor Slow pulse Apnoea Gasping Recession
Using oliguria as measurement in neonates
Amount of urine shows potential issues with blood volume (hypovoleamia)
What causes sepsis in neonates? 3 routes, potential bugs
Congenital
Early onset
Late onset
Group B step (70%)
Listeria
Gram negative organisms
Potential treatments for sepsis
Penicillin / gentamicin
Cefotaxime / ampicillin
Signs of sepsis in neonates
Often different from adults - temperature may be LOW, WC may be low, fever, poor feeding, vomiting, pallor, tachypnoea, sleepiness, irritability
Management of sepsis - steps
Investigate
Resuscitate
Antibiotics
Prepare for consequences (ventilation, fluids, coagulopathy, inotropes)
What causes birth asphyxia
IUGR (intrauterine growth restrictiion) Prematurity Abnormal CTG (cardio tosograph) Abnormal fetal blood gas Difficult delivery
Grading birth asphyxia (3)
Grade 1 - irritability, poor feeding
Grade 2 - fits, bad feeding, hypertonia
Grade 3 - floppy, intractable seizures, apnoea
Describe the window of opportunity to prevent cell death following asphyxia
Cells death follows asphyxia by about 24 hours, cooling a baby (early on, 6 hours) with moderate asphyxia can help prevent cell death
What are the four components of RDS
Weak chest wall
Excess lung liquid
No blood-air approximation
Surfactant deficiency
Describe meconium aspiration syndrome
Baby aspirates meconium (pre-natal faeces) during birth, which can cause respiratory distress, infection
Describe polyhydramnios
Can’t swallow fluids
Signs of abdominal emergencies
Can present with specific or non-specific features - distension, billous vomiting, obvious loops or protrusions
Potential causes of abdominal emergencies
NEC, malrotation, volvulus, Hirshsprung’s disease
Outline the duct dependent heart defects (5)
Pulmonary atresia, critical pulmonary stenosis, critical coarctation, transposition of the great arteries, hypoplastic left ventricle
Important principles of neonatal ventilation (2)
Functional residual capacity - xxx
Minute volume - xxx
Relationship between PIP and PEEP
PIP-peak inspiratory pressure
PEEP-positive end-expiratory end pressure
