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Medicine year 3 > neonatal > Flashcards

neonatal Flashcards

1
Q

when is surfactant produced

A

betweeen 24 and 34 weeks gestation

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2
Q

why is there a fall in pulmonary vascular resistance when a baby takes its first breath and how does this lead to closure of the foramen ovale.

A

the first breath expands the alveoli - decreasing pulmonary vascular resistance

which causes a fall in RA pressure and at this point the LA pressure is greater (squashing the atrial septum and causing closure of the foramen ovale)

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3
Q

why does the ductus arteriolus close after birth

A

prostaglandins are required to keep it open

increased 02 causes a drop in circulating prostaglandins

causing closure

becomes the ligamentum arteriosum

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4
Q

why does the ductus venous stop functioning after birth

A

the umbilical cord is clamped and there is no blood flow in the umbilical veins

structurally closes a few days later and becomes the ligamentum venosum

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5
Q

when are inflation breathes given

A

when the neonate is grasping or not breathing adequtely despite stimulation

  1. two x (5 inflation breaths lasting 3 seconds)
  2. heart rate low - 30 seconds of ventilation breaths
  3. chest compressions co-ordinated with ventilation breaths
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6
Q

resus procedure in neonates

A
  1. warm the baby
  2. APGAR score (0-10 , higher is better)
  3. stimulate breathing (place head in neutral position, drying with towel)
  4. check for meconium/obstruction
  5. inflation breaths
  6. chest compressions 3:1
  7. severe - therapeutic hypothermia
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7
Q

when are chest compressions used in neonate

A

HR < 60 despite resuscitation and inflation breaths

3:1 ratio with ventilation breaths

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8
Q

why might it be good to delay clamping to umbilical cord in neonates

A

allows more time for blood to enter the circulation of the babies - improve Hb, iron stores and blood pressure is reduced in intraventicular haemorrhage and necrosting enterocolitis

  • negative - increased neonatal jaundice - requiring phototheraphy
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9
Q

what vitamin is given after birth

A

vitamin K

babies are born deficient in vitamin K - important part of blood clotting

via IM injection in thigh (also helps stimulate cry) - explands the lungs

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10
Q

when is blood spot screening carried out

A

day 5

  • heel prick
  • screens for 9 conditions (CF, sickle cell, congenital hypothyroidism, phenylketonuria ….

come back in 6-8 weeks

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11
Q

when is newborn examination carried out

  • is a screening tool
A

72 hours after birth - (trainined midwife or doctor)

repeated 6-8 weeks by GP

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12
Q

where is the ductus arteriosus located?

A

arch of the aorta - and connects the pulmonary artery

stops functioning 1-3 days after birth

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13
Q

what to do if clinky/clunky sounds in hips of neonate

A

USS

to rule out development dysplasia of the hip

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14
Q

erbs palsy is a result of injury to what nerves

A

C5/C6 nerves

-> internally rotated shoulder
-> extended elbow
-> flexed wrist

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15
Q

what is caput succedaneum

A

traumatic birth
-> odema collects on scalp (outside the periosteum)
-> is able to cross sutures and usually mild or no discolouration of skin
- resolves in few days

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16
Q

what is cephalohaematoma

A

blood collects underneath the perisoteum but not within the skull

result of traumatic birth

blood does not cross * suture lines

blood can cause discolouration

usually resolves without treatment - might be anaemia and juandice due to blood that collects and breaks down

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17
Q

most common cause of neonatal sepsis

A

GBS***

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18
Q

risk factors for neonatal sepsis

A

GBS in mother

GBS previous baby

chorioamnionitis or fever > 38

prematurity < 37

early PROM or prolonged ROM

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19
Q

antibitoics used in sepsis in neonates

A

benzylpenicillin/gentamycin

***cefotraxime (lower risk)

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20
Q

what is hypoxic ishcaemic encephalopathy

A

lack of oxygen during birth - there is a lack of blood flow to tissues which affects the brain

ischaemic brain damge

(cerebral palsy/death)

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21
Q

potential causes of HIE (hypoxic ischaemic encephalopathy)

A

anything that leads to reduced oxygen to brain
-APH
- prolasped cord
- maternal shock
- nuchal cord (wrapped around neck)

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22
Q

symptoms of HIE

A
  • poor feeding, irritability, hyper alert (mild)
  • poor feeding, lethargic, hpotonic and seizures (cerebral palsy) - moderate
  • reduced consciousness, apnoeas, flaccid , reduced or absent reflexes (high mortality and death)
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23
Q

what is therapeutic hypothermia

A

babies who are near or at term can benefit if they have HIE

  • cooling baby - to 33 - 44C for 72 hours

to reduce inflammation and neurone loss after acute hypoxic injury

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24
Q

the main cause of neontal jaundice

A

physiological (mild from Day 2 - 7)

resolves day 10

  • high concentration of fragile RBC
  • less developed liver function

lots of RBC broken down/but liver is not conjugated faster

more dramatic in neontates -> immature liver

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25
what is kernicterus
brain damage due to high levels o biliruben in the blood
26
why are breast fed babies more likely to become jaundice
components of breast milk inhibit the ability of liver to process biliruben more likely to become dehyrated if not feeding adequetely - (slow passage of stools, increasing absorption of bilirubin in the intestines)
27
what is haemoltyic disease of the newborn
causes haemolysis - increased biliruben in the blood caused by incomptibility (rhesus antigens on mother verus foetus) *rhesus antigens* - > rhesus D antigen rhesus D negative (do not have the D antigen) -> will attack rhesus D positive (have D antigen on RBC)
28
what is prolonged jaundice
> 14 days in full term > 21 days in preterm -> prompt further investigation (look for biliary atresia , hypothyroidism, G6PD deficiency)
29
why treat neonatal jaundice
phototheraphy (blue light*/exchange transfusions -> precent kernicterus (present with less responsive, floppy, drowsy baby with poor feeding) -> cerebral palsy, deafness and CNS damage
30
features of necrotising enterocolitis (symptoms)
- pre-term neonates** bilous vomit bloody stools absent bowel sounds
31
test findings on imaging for necrotising enterocolitis
bloods - metabolic acidosis due to systemic compromise Abdominal XR - dilated asymmetrical loops of the bowel - bowel wall oedema - thumbprinting - pneumonitis intestinalis - GAS in the bowel
32
prematurity is birth before
< 37 weeks
33
prophylactic treatment for mothers who have a history of preterm birth or USS showing cervical length of 25mm or less before 24 weeks gestations?
* prophylactic vaginal progesterone (supositary) * prophylactic cervical clerage (suture)
34
treatment when preterm labour is suspected or confirmed
1. tocolysis - nifedipine (CCB) 2. maternal corticosteroids - before 35 weeks 3. IV magnesium sulphate (before 34 weeks - protect brain) 4 delayed cord clamping or cord milking - increase blood volume and haemoglobulin
35
what is apnea of prematury
breathing stops for more than 20 seconds (spontaneous) or shorter periods with oxygen desaturation and bradycardia common in premature neonate term - usually underlying pathology
36
causes of apnea in neonates
immaturity of autonomic nervous system - that controls RR and HR
37
management of apnea of prematurity
apnea monitoring tactile stimulation - prompt to start breathing IV caffiene*** to prevent apnoea and bradycardia if having recurrent episodes settle as baby grows and develops
38
what is retinopathy of prematurity
preterm and low birth weight babies < 32 weeks abnormal development of blood vessels in the retina can lead to scarring, retinal dettachment and blindness | retinal blood vessel development comple 37-40 weeks
39
why does reintopathy occur in premature babies
blood vessel grow is stimulated by hypoxia in utero when born - supplmenetal oxygen -> neovascularisation (abnormal blood vessels then regress and leave the retina without a blood supply) screened in babies in premature babies < 32 weeks
40
when does RDS usually occur
in babies born before 32 weeks gestation
41
CXR of babies with RDS
ground glass appearance
42
complications of RDS in babies (ST)
atelectasis (lung collaspe) inadequte gas exchange - hypoxia pneumothorax apnoea intraventricular haemorrhage necrotising enterocolitis
43
long term complications of RDS
chronic lung disease of prematurity retinopathy of prematurity neurological , hearing and visual impairments
44
management of RDS in neonates
antenatal - dexamethasone intubation/ventilation - if severe endotracheal surfactant (delivered via endotracheal tube) CPAP supplementary 02 - (maintain 92-95)
45
what is broncho-pulmonary dysplasia
chronic lung disease (CLD) of prematurity - when - infant requires oxygen theraphy beyond 36 weeks - changes on XR
46
how to prevent chronic lung disease of prematurity
corticosteroids - betamethasone at signs of premature labour CPAP rather than intubation/ventilation use caffiene to stimulate respiratory effort not over oxygenating with supplementory oxygen (aim 92-95%)
47
what are children bronchopulmonary dysplasia (chronic lung disease of prematurity) given to reduce risks of infection
palivizumab injections (given monthly in babies with chronic lung disease to prevent RSV) monoclonal antibody
48
what is necrotising enterocolitis
affects PREMATURE neonates part of the bowel becomes necrotic life threathening emergency death of bowel tissue - can lead to bowel perforation perforation -> peritonitis and shock
49
risk factors for necrotising enterocolitis
low birth weight prematurity RDS and assisted ventilation sepsis PDA/congenital heart disease
50
presentation of necrotising enterocolitis
intolerance to feeds vomiting - green bile distended , tender bowel blood in stools peritonitis and shock -> severely unwell
51
what will capillary blood gas show in necrotising enterocolitis
metabolic acidosis
52
what will abdominal XR show in necrotising enterocolitis
taken in supine position +/- lateral side - dilated bowel loops - bowel wall oedema (thickened bowel walls) ***- pneumatosis intestinalis - gas in bowel wall*** - pneumoperitoneum -> free gas in the peritoneal cavity and indicates perforation - gas in portal veins
53
inital management of necrotising enterocolitis while waiting on surgery
* nil by mouth * IV fluids * total parenteral nutrition * antibiotics surgery -> stoma
54
characteristics of fetal alcohol syndrome
(preterm, small for date, miscarriage) - small head (mirocephaly) - thin upper lip - smooth flat philtrum (groove between nose and upper lip) - short palpable fissure (distance from one side of eye to other) - hearing /vision
55
features of congenital rubella syndrome
congenital catarcts PDA and pulmonary stenosis Hearing loss
56
if in doubt mother has previously had the chicken pox
check IgG levels for VZV positive - immune if not - vaccine before or after pregnancy
57
what to do if mother is not immune of chicken pox - what is the prophylactic treatment
IV varicella immunoglobulins (within 10 days of exposure)
58
what to do if chicken pox starts in pregnancy (Treatment)
oral acyclovir - if present within 24 hours and > 20 weeks
59
features of congenital varicella syndrome
if infection in first 28 weeks of gestation - small head - growth restriction - significant skin changes following dermatomes - limb hypoplasia -
60
features of congenital toxoplasmosis infection
TRIAD - 1. intracranial cacification 2. hydrocephalus 3. chorioretinitis
61
when does sudden infant death syndrome occur
within the first 6 months of life
62
risk factor for SIDS - sudden infant death syndrome
- prematurity - low birth weight - smoking during pregnancy - slight risk when male
63

Medicine year 3 (38 decks)

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