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Infant Transport Team > CCP S3 shit > Flashcards

CCP S3 shit Flashcards

1
Q

Define fetal macrosomia

A

Larger than average newborn torso size. Commonly size with diabetic mothers. These newborns are considered LGA

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2
Q

what percentage of newborns require resuscitation?

A

10% require some degree

<1% require extensive resus

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3
Q

when does bronchopulmonary epithelium begin producing fetal lung fluid

A

bronchopulmonary epithelium beings producing liquids as early as the 6th week of gestation. The volume and rate at which liquid is secreted are calibrated to maintain lung volume at the desired FRC.

  • Issues such as congenital diaphragmatic hernia compress the lung in utero, preventing lung development in utero
  • Reduction of amniotic fluid (sucks as in prolonged ROM) results in hypoplasia of the lungs from reduction of volumes available for inhalation
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4
Q

What is the “one-third rule”

A

The fetal lungs secrete Na and fluid to cause the lungs to expand and promote growth during development

During birth: before and during birth the bronchopulmonary epithelium Na channels changes from secretion to absorption of Na and fluid. This is upregulated with glucocorticoids and epinephrine during delivery. The “squeeze” from the birth cannel aids in compressing the chest and dispersing more fluid

1/3 from Na channel changes from secretion to absorption of Na and fluid. Upregulated with catecholamines.

1/3 squeezed in vaginal delivery

1/3 from initial cry

Infants born preterm have not yet facilitated the initial 1/3 of fluid clearance.

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5
Q

what is the role of glucocorticoids in the antenatal preterm pregnancy

A

glucocorticoids accelerate the production of type 1 and type 2 alveolar cells. Type 2 alveolar cells produce surfactant. They also enhance the exposure of Na-K-ATPase which assist in fetal lung fluid clearance.

Steroids also provide neuroprotection and maturation of skin

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6
Q

Why is 24 weeks GA typically the cutoff for extrauterine fetal survival?

A

Alveoli aren’t developed at this GA, the majority of the lung is composed of terminal bronchi. Alveoli develop in the 3rd trimester and dramatically increase up to age of 2 then gradually to age 8

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7
Q

Betamethasone and dexamethasone dosages for antenatal corticosteroid

A

Betamethasone = 12mg x 2 q 24 hours apart

Dexamethasone = 6mg x 4 doses 12 hours apart

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8
Q

When are antenatal corticosteroids indicated?

A

<34 weeks

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9
Q

What 4 questions should be asked of the mother during imminent birth?

A

GA
ROM
Clear amniotic fluid
Complications

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10
Q

Explain chest wall physiology of an infant

A

Increased chest wall compliance results in the in-drawing of the chest wall during negative pressure inspiration. This is why see-saw repirations are normal for infants.

Infant respiration relies almost solely on the strength of the diaphragm

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11
Q

what is normal FRC of an infant

A

30ml/kg

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12
Q

how long is induction/ceaserian typically delayed once antenatal corticosteroids are administered?

A

One week

Benefits are seen as of 4 hours post-initiation of therapy but greatest after one week

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13
Q

What are the contributing factors to the fall of PVR

A
  • increase in alveolar and arterial oxygen tension. Fetal pulmonary circulation becomes more responsive to the vasodilator effect of oxygen after 31 weeks.
  • Increase in production of vasodilators
  • rhythmic distension of the lungs
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14
Q

When does the ductus arterioles normally close?

A

Within 12 hours of birth. Closure is primarily caused by redirection of BF to the pulmonary vasculature

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15
Q

What medication is used to maintain PDA patency

A

Prostaglandin. Alprostadil exerts direct vasodilatory effects on venous and ductus arterioles smooth muscle

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16
Q

Explain regulation of pulmonary vasculature tone

A

NO is produced by the endothelium and is metabolized into cGMP which produces vasodilation.

cGMP is degraded into GMP by the enzymes PDE5. cGMP degradation can be reduced by PDE5 by PDE5 inhibitors such as sildenafil

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17
Q

where are pre and post ductal measurements obtained from?

A

Pre-ductal is always from the right hand
Post-ductal should be from the feet because the left hand be pre-ductal in some circulation anomalies

Pre-ductal measurements identify the oxygenation of blood leaving the left ventricle before deoxygenated blood mixing from the RVA through patent PDA

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18
Q

What is the most effective way to determine GA?

A

Ultrasound. Accuracy worsens as the fetus develops

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19
Q

What is the most common organism to cause neonatal sepsis

A

Group B strep

E.Coli is the 2nd most common cause

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20
Q

What does blood in the amniotic fluid typically indicate ?

A

placental abruption

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21
Q

What are the two most common causes of premature fetal delivery

A

infection

cervical incompetence

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22
Q

What are the three most common causes of PTD without labour?

A

HTN
Fetal distress
Polyhydramnios

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23
Q

Why do we give Magnesium to preeclamptic mothers?

A

Prevent seizure of the mother (thought to be from NMDA receptor action, increasing the threshold for seizure)

Fetal neuroprotection (unknown mechanism)

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24
Q

What is lanugo

A

Newborn body hair. More prominent in early pregnancy

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25
Q

What is considered term?

A

> 37 weeks

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26
Q

what is considered preterm

A

23-36+6

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27
Q

what is considered post term

A

> 41

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28
Q

Define asymmetric IUGR

A

Hypotrophic growth restriction that is head sparing. The undernourished fetus directs energy to maintain vital organs (brain/heart)

Related to maternal issues. The baby usually catches up in growth

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29
Q

Define symmetric IUGR

A

Entire growth is restricted, considered SGA with a head that is appropriate for the body size.

Related to maternal issues. The baby doesn’t usually catch up with growth

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30
Q

Explain why IUGR babies are at risk of hypoglycaemia and hypothermia

A

IUGR babies have reduced body fat comparative to high body surface area. They also have hypo plastic livers

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31
Q

What is colostrum

A

the first breast milk produced by the mammary glands that are rich with immunologic factors

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32
Q

What is the Fenton chart

A

it is used by BCCH to track and assess a newborns growth

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33
Q

whats the percentage of body water in a newborn

A

Up to 85%

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34
Q

What is the difference between distribution of fluid between a preterm and a term infant?

A

term = 50% intravascular and 50% ECF

Preterm= primarily intravascular

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35
Q

What is normal UO of an infant

A

2-4 ml/kg/hr

new borns have very low UO for the first 24 hours then diurese

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36
Q

Three disabilities of preterm kidneys

A
  1. decreased GFR
  2. decreased reabsorption of Na and HCO3
  3. Decreased ability to dilute or concentrate urine
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37
Q

Six factors contributing to increased insensible water losses

A
  1. Lower gestation (due to high body surface area and immature water permeability skin)
  2. skin defects (gastrochisis)
  3. high body or ambient temperature (3% per degree)
  4. radiant light (50% increase IWL)
  5. increased motor activity
  6. pathogenic (chest tube etc)
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38
Q

5 Ways we can reduce insensible water losses:

A
  1. double walled incubator or plastic heat shield
  2. increase ambient humidity
  3. plastic bags
  4. humidified cpap/vent
  5. antenatal corticosteroids to promote maturation of skin and kidneys
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39
Q

over what time do newborns typically lose weight and gain it again

A

lose the first 2-3 days then gain by 7-10 days

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40
Q

what are two causes of hyponatremia in a newborn

A

SIADH

Excessive maternal free water intake

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41
Q

Two causes of hypernatremia in new borns

A

excessive sodium intake

dehydration

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42
Q

causes of hypokalemia in neonates

A

excessive GI losses

dilution

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43
Q

What weight should we use for medication dosing in the newly born infant?

A

birthweight until weight losses are regained

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44
Q

What is a repogle tube

A

A double lumen tube that allows for suctioning co-comittantly with feeding

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45
Q

what does APGAR stand for

A 
activity
pulse
grimace
appearance
respiration
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46
Q

When does the cough reflex become more evident

A

At one or two months of age.

this is when we begin seeing coughing with respiratory infections

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47
Q

Until what age are infants obligate nose breathers?

A

6 months

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48
Q

What age is bronchiolitis most common in?

A

<2 years of age (but especially below 6 months)

Bronchiolitis is unresponsive to bronchodilators

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49
Q

Some of the neurological differences seen in children

A
  • suture and fontanelles (which close around 6 months)

- spinal cord ends at L3 (L1-L2 in adults)

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50
Q

List some CVS differences seen in children

A
  • stroke volume is fixed, HR is the only way to increase CO

- SVT is more common in the first few weeks of life because of the immaturity of the AV septum

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51
Q

List some of the respiratory differences seen in children

A
  • cone shape narrow trachea
  • larger tongue
  • softer pallate
  • lower FRC (contributing to quicker desaturations, along with increase basal metabolic rate
  • immature sinuses
  • toothless but at risk of tooth bud injury
  • obligate nose breathers
  • compliant chest wall
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52
Q

List some of the dermatological differences seen in children

A
  • thin skin and higher body surface area contribute to hypothermia
  • brown fat is utilized for thermogenesis, rather than shivering
  • sweating and vasodilation is less effective in infants and toddlers
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53
Q

Why is SCIWORA more common in infants

A
  1. the fulcrum is located at C1/C2 rather than C5-C6 in adults
  2. Atlantoaxial dissociation is more frequent and is fatal
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54
Q

Three components of paediatric triangle

A

apperance
breathing
circulation

55
Q

What is the equation for average MAP in children

A

age x 1.5 +40

56
Q

A HR of up to ___ is useful to increase CO in children. Beyond this rate, diastolic filling is impaired

A

180 HR

57
Q

what are the two most troublesome side effects of Dexmedetomidine (precedex)

A

Bradycardia and hypotension

58
Q

Why is propofol not used beyond 24 hrs in the sedation of pediatrics

A

-childreen are at higher risk of PRIS due to fat distribution and dosage requirements for effects

59
Q

outline the drug profile of Milrinone

A

classified : Phosphodiesterase inhibitor

MOA: increases intracellular cAMP, increasing cardiac isotropy, and chronotropy, dromotropy

60
Q

Why does epinephrine cause hyperlacataemia

A

thought to be caused by peripheral vasoconstriction of distal capillaries with some degree of distal limb ischemia

61
Q

What is a histogram

A

a graph that is used to determine time at a specific oxygen saturations

62
Q

List the fetal channels

A 
umbilical veins
ductus venosus
foramen ovale
ductus arteriosus
umbilical artery
63
Q

Describe TTN

A

Respiratory distress associated with inadequate fetal lung clearance. Transient in nature, and generally resolves in 24 hours

64
Q

Describe neonatal RDS

A

Respiratory distress caused by surfactant deficiency

65
Q

Describe PPHN

A

Pulmonary HTN caused by abnormal presence of elevated PVR that leads to right-to-left shunting of deoxygenated blood though the PFO and PDA.

PPHN is often caused by underdevelopment of pulmonary vascular bed, and can also be caused by fetal distress, such as in MAS

66
Q

Define meconium aspiration syndrome

A
  • fetal distress results in meconium with subsequent aspiration. Meconium layers the respiratory tract, causing chemical irritation, inflammation, infection and surfactant inactivation
  • MAS produces bilateral diffuse grossly patchy opacities. The areas of thee CXR are patchy because of areas of total atelectasis, as well as areas of air trapping within the alveoli
67
Q

Why is meconium voided during fetal distress

A

increased vagal outflow from umbilical cord compression or increased sympathetic outflow from hypoxia causes peristalsis and relaxation of the anal sphincter

68
Q

what is the equation for calculation ETT size in peds?

A

age/4 + 3 = cuffed

age/4 + 4 = uncuffed

69
Q

What is the calculation for ETT depth

A

tube x 3

70
Q

what is the neonatal/ped does for succinylcholine for RSI

A

2mg/kg

71
Q

Why are babies born from diabetic mothers at higher risk of hypoglycaemia

A

The fetus is accustomed to receiving an abidance of glucose, meaning they have had to up regulate endogenous insulin production in order to maintain normoglycemia.

Once the placental delivery of glucose comes to a halt, the infant will be overproducing insulin for the amount of glucose being produced

72
Q

what are three clinical features necessary for the dx of DKA

A

Hyperglyemia >11.1 mmol/L
pH <7.3
HCO3 <15
Ketones

73
Q

Why does gluconeogenesis and glycogenolysis occur during DKA despite elevated BGL?

A

Astrocytes cannont detect glucose levels because of insulin deficiency. Without insulin to transport glucose into astrocytes, the brain registers hypoglycaemia, and promotes gluconeogenesis and glycogenolysis

74
Q

What are the three ketones?

A
  • Acetoacetate
  • Beta-hydroxybutrate
  • Acetone
75
Q

Outline the mgmt of DKA in peds

A
  • fluid 10-20ml/kg
  • even rehydration over 24-36 hours, assuming 5-10% dehydration
  • use 0.45 or 0.9 NaCl
  • No insulin for the first 1-2 hours of treatment, due to increased risk of cerebral edema that is likely related to fluid channels in the brain
  • target BGL 8-12mmol/L with continuous insulin infusion once initiated, using 2-bag method with glucose to match
  • continue insulin therapy until anion gap or BOHB levels resolve
  • Potassium correction in conjunction with insulin therapy
76
Q

Explain the fluctuation of sodium in DKA

A

Hyponatremia is caused by water shift into the ECF, diluting serum sodium

Hypernatremia is superimposed from loss of water with glucosuria-induced osmotic diuresis, sparing sodium and potassium

77
Q

describe mechanism that produce hyperkalemia in DKA

A
  1. solvent drag
  2. impaired K entry into cells from insulin deficiency
  3. intracellular protein and phosphate depletion
  4. buffering of hydrogen ions
78
Q

Criteria for dx of HHS

A

BGL >33.3 mmol/
Hyperosmolarity >320 mOsm/kg
small or absent ketonuria
absence of significant acidosis

79
Q

outline mgmt of HHS

A

fluids 20ml/kg NS

correct glucose, potassium and sodium levels

  • glucose lowered by 3-5 mmol/Hr
  • Sodium lowered by 0.5mmol/Hr
80
Q

What is the marker of the correction of HHS

A

-osmolality and glucose back to normal ranges

81
Q

what is the dose of d10w for neonatal hypoglycaemia

A

2ml/kg bolus followed by 4ml/kg/hr infusion

82
Q

List four predisposing factors to PTD

A

Cervical shortening
Incompetent cervix
PPROM
Preterm labour

83
Q

RF for PTD

A

Maternal - previous PTD, uterine abnormality

Fetal – IUGR, fetal anomaly, multiple gestation

Placental - poor implantation, antepartum hemorrhage

84
Q

what is considered a short cervix

A

<2.5cm before 24 weeks

85
Q

what is an incompetent cervix

A

it is essentially the opening of the cervix without labour. defined as painless cervical dilation, typically before 24 weeks GA

86
Q

What are the components of the initial assessment of PTL?

A
  • GA
  • Palpation of contractions
  • sterile speculum exam
  • digital exam
87
Q

What is fFN testing

A

-fetal fibronectin testing is a protein dectable during labour. it is produced when there is separation of the placenta from the uterine wall

The negative predictive value is very good at ruling out PTL

88
Q

Goals of tocolytic therapy ?

A

allow for steroids to work
allow for abx to work
transport

89
Q

what is a normal fetal HR

A

110-160

90
Q

What are the consequences of PROM

A

PTD within 1 week in 50% of births,
Fetal pulmonary hypoplasia
Fetal skeletal maldevelopment
Ascending infection

91
Q

What are the steps of delivery of a fetus with shoulder dystocia? (theres an acronym)

A
  • Ask for help
  • Legs back
  • Anterior shoulder (push anterior shoulder downwards, just above pubic bone)
  • rotate
  • manual removal of posterior arm

ALARM

92
Q

what medication reduces preeclampsia by ~50%

A

Aspirin

93
Q

Define HTN in pregnancy

A

<140/90

94
Q

Severe HTN in pregnancy

A

SBP or DBP >160/110

95
Q

Define gestational HTN

A

non-preexisting hypertension that develops beyond 20 weeks GA

96
Q

What are the criteria needed for dx of preeclampsia

A

Gestational HTN with 1 of the following:

- new proteinuria or associated symptoms

97
Q

Define oligohydraminos

A

Deficiency of amniotic fluid

98
Q

What are the benefits of delayed cord clamping?

A
  • increased blood volume (20-40ml/kg)
  • increased stem cell transfer
  • increased iron volume
  • increased oxygen carrying capacity
  • decreased risk of NEC
  • decreased risk of IVH (likely due to stabilized BP from additional blood volume)
99
Q

When is delayed cord clamping contraindicated?

A

Absent blood flow to neonate

Multiple gestations that are sharing a placenta (though can be utilized on last baby)

100
Q

define parturition

A

the active of giving birth to the young

101
Q

define Braxton hick contractions

A

unorganized contractions of the uterus

102
Q

List four factors that promote labour

A
  • fetus
  • myometrial activation
  • hormones
  • ROM
103
Q

How does ROM induce labour

A

ROM produces an inflammatory cascade mediated by arachidonic acid that ultimately thins and dilates the cervix

104
Q

What are tocolytics

A

a medications used to suppress premature labour

105
Q

What are the commonly used tocolytics

A

Nifedipine (Adalat) – CCB. Blocks calcium influx to inhibit labour contractions

Indomethacin –> an NSAID and tocolytic that inhibits prostaglandin synthestase

Progesterone

106
Q

Why is Nifedipine usually the first tocolytic agent used at BCCH

A

it has less adverse effects on thee DA and less risk of causing NEC

107
Q

Explain the MOA of oxytocin

A

Oxytocin is classified as a uterotonic
Oxytocin stimulates uterine contraction by increasing intracellular calcium.

Oxytocin is released from the posterior pituitary during active labour. It is useless when cervix is full constricted (as it essentially produces uterine contractions against a closed door)

108
Q

What is the role of tocolytics in preterm labour

A

Tocolytic delay labour to allow prelabour growth. They also allow for administration of corticosteroids to allow fetal production of surfactant and to buy time for transport.

109
Q

What are the four stages of labour?

A

stage 1 - onset of regular contractions to full dilation

stage 2 - full cervical dilation to delivery of the fetus

stage 3 - delivery of the placenta

stage 4 - post birth

110
Q

When delivering the placenta, what are some important considerations?

A
  • delivery occurs with maternal effort and gentle cord traction
  • place a hand at the symphysis pubis to prevent uterine inversion
  • a placenta will normally deliver with a gush of blood, with cord lengthening from the uterus contracting downwards. uterus contractions clamps the closure of the ruptured blood vessels from the uterus
111
Q

What is the importance of immediate breast feeding after birth?

A

Oxytocin release, stimulating uterine contraction and reducing hemorrhage

Colostrum feeding for the infant

Conduction of heat from mother to infant

112
Q

What is the MOA of ultraviolet lights in babies with hyperbilirubinemia

A

Ultraviolet light acts as a catalyst for the binding to albumin, promoting elimination

113
Q

What are the most common cause of death in PTD

A

RDS. cerebral hemorrhage, NEC

114
Q

Risk Factors of PTD

A

Maternal –> previous PTD, pre-excisting disease, uterine anomaly

Fetal –> IUGR, fetal anomaly, multiple gestation

Placental –> poor implantation, antepartum hemorrhage

115
Q

What is considered a short cervix

A

<2.5 cm before 24 weeks

116
Q

Define PTL

A

PTL is defined as regular contractions twice in 10 minutes, as well as changes in length or dilation of the cervix.

117
Q

What are the components of the initial assessment of PTL

A

eGA
Palpitation of contractions
sterile speculum exam (cultures, rule out ROM, FFT)
VE

118
Q

What is ferning?

A

Microscopic investigation into fluid obtained from speculum exam. Presence of ferning indicates PROM

119
Q

Define gestational HTN

A

Non-preexisting hypertension that develops beyond 20 weeks GA

120
Q

What are the criteria needed for the dx of preeclampsia

A

Gestational HTN with 1 or more following:
- new proteinuria
or
-associated symptoms

121
Q

At what GA does preeclampsia/Eclampsia develop

A

> 20 weeks GA

122
Q

What is the pathophysiology of preeclampsia

A

Poor placentation results in inadequate development of placental blood flow. This results in release of antiangiogenic factors from the placenta into the maternal circulation, which binds with vascular endothelium growth factor, resulting in widespread endothelial dysfunction.

123
Q

Define HELLP syndrome

A

complication of preeclampsia involving hemolysis, elevated liver enzyme and low platelet count

124
Q

What symptoms should promote investigation into HELLP syndrome

A

Nausea/vomiting

RUQ pain

125
Q

Outline the mgmt of hypertensive disorders of pregnancy

A

Initial therapy –> Nifedipine and labetalol

Second line methyldopa and other BBs

126
Q

Why should ACE-i and ARBs be avoided in the mgmt of hypertensive disorders of pregnancy?

A

they’re fetotoxic

127
Q

Why does HTN often peak in the days following delivery

A

the return of volume from the uterus produces hypertension

eclampsia can occur up to 6 weeks post-partum

128
Q

define oligohydramnios

A

deficiency in amniotic fluid

129
Q

What is placenta accreta

A

Placental growth into the uterus. Placenta accreta is associated with massive mortality and hemorrhage

130
Q

What are the benefits of delayed cord clamping?

A 
increased blood volume (20-40ml/kg additional blood)
increased stem cell transfer
increased iron volume
increased oxygen carrying capacity 
decreased risk of NEC
Decreased risk of IVH
131
Q

disadvantages of delayed cord clamping

A

higher risk of jaundice, though minimal

132
Q

When is DCC contraindicated

A

Absent blood flow to neonate

multiple gestations that are sharing a placenta (though can be utilized on the last baby)

133
Q

CVS changes in moms

A

increased preload from a rise in blood volume. decreased afterload from declining SVR. increased HR ~20 BPM. Left axis deviation

134
Q

Resp changes in moms

A

progesterone stimulation produces an increased resp drive, reducing PaCO2 to 30-32 creating a respiratory alkalosis

PaO2 elevation to 104-108 as a result of increased CO and minimization of VQ mismatch. Upward displacement of diaphragm leading to 20% decrease in FRC. Oxygen consumption increases to 20%

Infant Transport Team (14 decks)

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