Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pediatrics > Perinatal Period > Flashcards

Perinatal Period Flashcards

1
Q

Gestational period:

preterm, term and post term?

A
  • preterm: less than 37 wks
  • term: 37-42 weeks
  • post: more than 42 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Neonatal and perinatal period?

A
  • neonatal: first 28 days of life (+preterm time period)

- perinatal: from 20 weeks gestation to one month after birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is involved in fetal-neonate transition?

A
  • cardiovascular transition
  • respiratory transition
  • temp maintenance
  • growth transition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

3 cardiovascular shunts in the fetus?

A
  • ductus venosus
  • ductus arteriosus
  • foramen ovale
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Ductus venosus - purpose?

A
  • connects umbilical vein to IVC
  • allows O2 blood directly from mom to enter circulation (bypasses liver) via IVC
  • disappears within 2 weeks after birth
  • becomes ligamentum venosum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Ductus arteriosus - purpose?

What happens at birth?

A
  • a channel of communication b/t the main pulmonary artery and the aorta
  • allows majority of blood which would enter pulmonary vasculature to bypass directly to the aorta
  • at birth: extremely sensitive to O2 content of blood, at birth increased O2 initiates constriction and subsequent closure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Foramen ovale - purpose?

A
  • opening b/t 2 atria of the fetal heart
  • allows O2 blood from mom which enters right atrium to be channeled directly to left atrium (R - L shunting) - onto LV, aorta and system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Diff in vascular resistance in uteror and at birth?

A
  • in utero: systemic vascular resistance is low
    pulmonary vascular resistance is high (lungs are full of fluid)
  • at birth: increased systemic vascular resistance, decreased pulmonary vascular resistance: this increases left atrial pressure which closes the foramen oval and eliminates R to L shunting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the last system to fully mature in utero?

A
  • pulmonary system
  • occurs during 3rd trimester (28-40 weeks):
    surfactant starts being produced, surfactant reduces surface tension and stabilizes alveoli, surfactant production is usually sufficient by 34 weeks gestation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Temperature maintenace at birth?

A
  • heat regulation isn’t well developed
  • sensitivie to excess heat loss and heat retention (hypo-/hyperthermia)
  • immediately after birth: dry the infant and provide radiant heat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Growth transition after birth?

A

loss of body weight:

  • occurs first few postnatal days
  • wt loss of 5-10% is normal in first week after birth
  • predominantly loss of extracellular water
  • inadequate nutritional intake

acclimation occurs:
- most newborns back to birth wt by 2 weeks of age, feeding improves, and growth accelerates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

APGAR?

A
  • Activity - 2 pt:active movement, 1: arms and legs are flexed
  • Pulse - 2: over 100 bpm, 1:below 100 bpm
  • Grimace - 2: active motion, 1: some flexion of extremities
  • Appearance - 2: completely pink, 1: body pink, extremities blue
  • Respiration - 2: vigorous cry, 1: slow, irregular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Impt basic principles of neonatal resuscitation?

A
  • O2!!!
  • bulb suctioning, particularly if meconium stained amniotic fluid
  • stimulation (induces sympathoadrenal mediated increases in respiratory and cardiac performance)
  • drying and warming for maintenance of thermoneutrality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Commonly screen conditions of newborn?

A
  • babies born with these conditions appear completely normal, so that is why we screen!
  • PKU
  • galactosemia
  • hemoglobinopathies
  • hypothyroidism: swollen tongue, puffy face, cold extremities, low muscle tone, poor feeding, lethargic
  • hearing screening
  • disorders usually only develop after baby has been feeding for 2-3 days.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What sizes is small for gestational age (SGA)?

A
  • below 10th percentile on growth chart

- this is diff than intrauterine growth retardation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What size is considered appropriate for gestational age (AGA)?

A
  • b/t 10th and 90th percentile on growth chart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What sizes are considered large for gestational age (LGA)? Most common cause of macrosomia?

A
  • above 90th percentile for wt on growth chart

- macrosomia: gestational diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Symmetric IUGR?

A
  • infant can be SGA due to genetics and is normal but small
  • symmetric implies event in early pregnancy such as chromosomal abnormalities. drug or alcohol use, or congenital viral infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Asymmetric IUGR?

A
  • only wt at or below 10th percentile
  • head is normal size, body is smaller
  • asymmetric implies problem late in pregnancy such as pregnancy induced HTN, pre-eclampsia or placental insufficiency
    (better outcome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Causes of LGA?

A
  • infant of diabetic mother
  • erythroblastosis fetalis (hydrops): Rh - mom with abs with Rh + baby
    -normal variants:
    genetic predisposition, male fetus, post-dates gestation, and multiparity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why is the infant of a diabetic mother usually large for gestational age and why is the baby at risk for hypoglycemia?

A
  • large because of increased amt of glucose it is receiving
  • at risk for hypoglycemia because it was so used to receiving extra glucose that stimulated increase production of insulin as well - at birth not exposed to hyperglycemia - hypoglycemia state
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Why should all LGA infants be screened for hypoglycemia while in the hospital?
What are abnormal levels of glucose?
signs of hypoglycemia?

A
  • b/c hypoglycemia can occur w/in 3 hrs of birth
  • at 3 hrs of life normal term babies blood glucose stabilizes at 50-80 mg/dl
  • concentrations below 40-45 mg/dL after first few hours of life should be considered abnormal
  • heel stick to screen, if low or borderline, need direct measurement of blood
  • Continued surveillance until full enteral feedings without IV supplementation for 24 hr period
  • signs:
    lethargy, poor feeding, irritability, termulousness, jitteriness, apnea, and seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Tx of IDM hypoglycemia?

A
  • IV glucose
  • dose depends on level of hypoglycemia and whether there are sxs
  • if infant is alert and vigorous and only mildly hypoglycemic, may just feed and monitor carefully
  • ## prognosis usually excellent if therapy is prompt
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why would IUGR infants have hypoglycemia in some cases?

A
  • due to reduced glucose stores
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Normal newborn RR?

A
  • 30-60
26
Q

What is respiratory distress syndrome?

A
  • pulmonary system is last to fully mature
  • epithelial cells in alveoli called type II cells produces surfactant
  • surfactant lowers surface tension
  • surfactant deficiency leads to markedly decreased lung compliance
  • uncommon at 37 weeks gestation and beyond
  • 70% chance of RDS at 28-30 weeks gestation
  • hypoxemia and acidosis contribute to pulmonary vasoconstriction - leads to increased pulmonary vascular resistance - blood will shunt away from these areas of lungs
27
Q

Signs of RDS? What will you see on CXR?

A 
- within 6 hrs of birth:
tachypnea
retractions
nasal flaring
grunting 
cyanosis
  • on CXR:
    reticulogranular pattern (ground glass)
    air bronchograms
28
Q

DDx of Respiratory disorders?

A
  • sepsis
  • pneumonia
  • pneumothorax
  • mass-occupying lesions in chest (stomach herniating into chest through diaphragm)
  • polycythemia
  • transient tachypnea of newborn
29
Q

Management of RDS?

A
  • O2 therapy with monitoring of blood gases
  • CPAP
  • mechanical ventilation (if needed)
  • artificial surfactant replacement
30
Q

What is meconium aspiration syndrome (MAS)?

signs?

A
  • staining of amniotic fluid with meconium in assoc with respiratory distress
  • more common the longer the gestation (theory: fetal distress leads to meconium passage in utero followed by aspiration from gasping)
  • **obstructive disease
  • most common with postmaturity and fetal distress
  • signs:
    grunting, nasal flaring, retractions, marked tachypnea, and varying degrees of cyanosis (similar to RDS)
31
Q

What will you see on CXR, ABGs in MAS?

A
  • CXR reveals fluffy infiltrates with alternating areas of lucency
  • pneumothorax or pneumomediastinum and hyperinflation with flattening of diaphragm often seen
  • ABGs reveal hypoxemia (low O2) and hypercarbia (high CO2) - respiratory acidosis
32
Q

Management of Meconium Aspiration Syndrome?

A
  • suctioning of nose and oropharynx after delivery of the head should be done by obstetrician when meconium staining is present
  • chest physiotherapy
  • CPAP or mech ventilation
  • routine admin of abx b/c of possible occurrence of secondary bacterial pneumonia
33
Q

What is Persistent Pulmonary HTN of newborn (PPHN)?

A
  • also known as persistent fetal circulation:
    pulmonary HTN, R to L shunting of desaturated blood through fetal pathways (PFO or PDA) in structurally normal heart
  • caused by sustained elevation in pulmonary vascular resistance
  • can be idiopathic or secondary to RDS, congenitatl diaphragmatic hernia, hyperviscosity, sepsis, or other causes
  • echo with color flow doppler can demonstrate R to L shunting pattern and rule out structural heart defects
34
Q

What is TTN?

What does CXR show?

A
  • transient tachypnea of the newborn:
    retained lung fluid
    distress typically from birth
    reqrs mild to mod O2 (25-50%)
    -often occurs in term or near term infants
  • CXR shows perihilar streaking and fluid in interlobar fissures
  • resolution usually occurs within 12-24 hrs
35
Q

Physiology of Jaundice:

Production and excretion

A
  • jaundice is caused by excessive levels of bilirunin in the bloodstream
  • porduction: bilirubin is produced from destruction of RBCs in liver and spleen
  • it is unconjugated and binds to albumin and is transported to the liver
  • excretion: conjugated in the liver, excreted in the biles, and eliminated in the urine and feces
  • any process that causes excess destruction of RBCs or interferes with bile excretion can cause hyperbilirubinemia
  • unconjugated bilirubin can pass through BBB
36
Q

Why do we care about jaundice?

A

because unconjugated (indirect) bilirubin is neurtoxic:
- bilirubin induced neuro dysfxn: BIND
- acute bilirubin encephalopathy (early signs of toxicity): neuro changes occur in first postnatal weeks, characterized by hypotonia and seizures, can be reversed unless levels of bilirubin remain elevated
- kernicterus:
chronic and permanent sequelae of BIND, develops during first year of life, can range from subtle to severe sxs

37
Q

Kernicterus? Occurs at what levels? Tx?

A
  • Chronic and permanent sequelae of BIND
  • can occur when unconjugated bilirubin exceeds binding capacity of albumin
  • it crosses BBB to damage cells of the brain
  • kernicterus can occur in full term newborns when unconjugated bilirubin levels are above 20-25 mg/dL
  • occurs at lower levels with premature infants
  • tx depends on circumstance and rate of bilirubin increase
38
Q

3 mechanisms that predispose newborns to physiologic jaundice?

A
  1. bilirubin production is higher:
    newborns have higher HCT (50-60%), fetal RBCs have shorter life span and there is greater turnover of RBCs
  2. bilirubin clearance by the liver is decreased due to decrease in enzyme - UGT1A1
  3. increased enterohepatic circulation: conjugated bilirubin (can’t be reabsorbed) reaches infant’s gut
    - B-glucuronidase in infant’s gut acts on bilirubin to make it unconjugated and then reabsorbed into circulation again
    - the infant gut has few bacteria in it to counter the effects of B-glucuronidase
39
Q

Progress of physiologic jaundice of the newborn?

A
  • begins after 24 hrs of life
  • peaks at level of 12-15 mg/dL of indirect bilirubin at around 3 days of life
  • returns to normal by days: 10-12
  • progresses cephalocaudally (head to toe)
  • premature infants may take 4-5 days to reach peak bilirubin levels, and these peaks may be twice that observed among full term infants
40
Q

At what serum bilirubin level does jaundice appear?

A
  • total bilirubin of 3-5

- this includes both direct and indirect

41
Q

Difference b/t direct and indirect bilirubin?

A
  • direct bilirubin has been conjugated (water soluble) by the liver
  • indirect bilirubin isn’t conjugated (not water soluble)
  • if an infant with physiologic jaundice it is INDIRECT bilirubin that is high b/c liver is immature and can’t conjugate bilirubin
  • In obstructive diseases - it is direct bilirubin that is elevated
42
Q

Purpose of indirect coomb’s test?

A
  • tests for presence of blood type abs in serum
  • pts serum is incubated with RBCs with known antigenic markers
  • if there are abs present in serum they will bind to RBCs
  • a positive test results in agglutination of RBCs
43
Q

What is exaggerated physiologic hyperbilirubinemia or breast feeding jaundice?

Tx?

A
  • jaundice is often exagegerated when the milk takes longer to come in
  • there is usually mild dehydration
  • newborns should feed at a min q 2-3 hrs
  • produce 6-8 wet diapers a day
  • 5-6 stools a day
  • Tx:
    frequent feeding and adequate hydration, depending on total serum bilirubin level:
    consider phototherapy (converts unconjugated bilirubin into water soluble forms that cna be excreted without conjugation in liver)
  • exchange transfusion if needed (rarely needed)
44
Q

Tx of jaundice?

A

phototherapy:

  • use a blue light of a particular wave length with as much skin exposed as possible with eyes covered
  • the light converts bilirubin to lumirubin which is excreted in the bile and urine
  • risks include retinal degeneration, dehydration, hyperthermia and at times rashes
  • monitor temp, hydration status, total bilirubin levels and time of exposure

Exchange transfusion:

  • used when phototherapy fails or an infant shows signs of BIND, including acute bilirubin encephalopathy (reversible) and kernicterus (irreversible)
  • rarely used
  • irradiated blood is used to reduce risk of graft vs host disease
45
Q

RFs of phototherapy?

A
  • G6PD deficiency
  • sig lethargy
  • temp instability
  • isoimmine hemolytic disease
  • albumin less than 3 g/dL
  • asphyxia
  • sepsis
  • acidosis
46
Q

How do you diff b/t physiologic from pathologic jaundice?

A
  • exaggerated physiologic jaundice occurs at serum bilirubin levels b/t 7-17 mg/dL
  • levels above 17 in full term infants aren’t considered physiologic and requier further investagation
  • jaundice isn’t considered physiologic if:
    onset in first 24 hrs,
    rate of increase of serum bilirubin exceeds 0.5 mg/dL/h
  • conjugated serum bilirubin exceeds 10% of total bilirubin or 2 mg/dL - obustructive problem
47
Q

increased production - causes of jaundice?

A
  • hemolytic disease: ABO or Rh incompatabilities
  • inherited RBC membrane defects
  • G6PD
  • sepsis causing hemolysis
  • increased RBC breakdown:
    cephalohematoma, polycythemia
48
Q

Decreased clearance - causes of jaundice?

A
  • inherited liver defects, such as gilbert syndrome (liver isn’t conjugated bilirubin as effectively)
49
Q

Increased enterohepatic circulation - causes of jaundice?

A
  • human milk jaundice
  • breast milk jaundice
  • impaired intestinal motility
50
Q

What is Caput Succedaneum?

A
  • present at birth on normal vaginal delivery
  • may lie on sutures, not well defined
  • soft, pits on pressure
  • skin ecchymotic
  • size largest at birth, gradually subsides within a day
  • no underlying skullbone fracture
  • no tx required
51
Q

What is ceaphalhaematoma?

A
  • appears within a few days after birth on normal or forceps delivery
  • well defined by suture, gradually developing, hard edge
  • soft, elastic but doesn’t pit on pressure
  • no skin change
  • become largest after birth and then disappears in 6-8 weeks to few months
  • may have underlying skull fracture
  • no tx reqd
52
Q

What is ABO hemolytic disease?

A
  • occurs in context of mom having type O and baby having A or B
  • preformed maternal anti-A or anti-B abs can passively cross placenta late in pregnancy or during delivery
  • abs attack A or B ag on fetal RBCs
  • about 25% of pregnancies have potential for ABO incompatibility, only around 10% of these (2.5%) develop hemolysis
  • disease usually isn’t severe
  • can accompany any pregnancy where mom is type O
  • sxs can appear in first 24 hrs
  • may develop sig anemia over first several weeks, may need to be transfused at a few weeks of age
53
Q

What is Rh hemolytic disease?

A
  • much less common but more severe
  • same process that occurs with ABO incompatibility but with abs directed against Rh protein
  • can be more severe with each pregnancy b/c mom built up abs to Rh protein (autoimmunized)
  • can accompany any pregnancy where mom has Rh - blood
  • sxs in first 24 hrs
54
Q

Rh hemolytic disease (Rh isoimmunization) - how can it be prevented? What happens in severe cases?

A

usually can be prevented using Rhogam:

  • immune globulin
  • admin to any Rh neg woman after any invasive procedure during pregnancy as well as after any miscarriage, abortion, or delivery of Rh + infant
  • impt b/c mother will never be sensitized to Rh+ antigen
  • ERythroblastosis fetalis (hydrops fetalis): occurs in severe cases, especially in Rh - women who haven’t received appropriate care with Rhogam previously
  • often results in fetal or neonatal death w/o appropriate prentatal intervention
  • less severe cases result in hemolysis with resultant hyperbilirubinemia and anemia
55
Q

Tx of Rh hemolytic disease?

A
  • when dx prenatally, transfusion of fetus with Rh (-) cells is done
  • following delivery, phototherapy is started immed with exchange transfusion as necessary
  • ongoing hemolysis will occur until maternal ab gone
  • infants should be carefully followed for 2 months to ensure they don’t become anemic enough to warrant further transfusions
56
Q

What is human milk jaundice? Tx?

A
  • prolonged unconjugated hyperbilirubinemia
  • uncommon
  • etiology unclear, may be assoc with b- glucuronidase, enzyme found in breast milk
  • lasts 3 weeks to 3 months in thriving infant w/o evidence of hemolysis or other disease
  • peaks at 10-15 days, with max bilirubin level of 10-30 mg/dL
    -tx:
    nursing is interrupted for 24-48 hrs
    bilirubin level falls quickly and won’t rebound to same level when nursing is resumed
57
Q

What is breast milk jaundice? Rfs?

Tx?

A
  • usually occurs when breastfeeding is difficult
  • occurs during first week of life
  • lactation difficulties lead to inadequate intake with wt loss and fluid loss leading to dehydration
  • this results in slower bilirubin excretion and increased enterohepatic circulation
  • RFs:
  • inadequate education from clinicians and lactation consults
  • inadeq documentaion of latching on by infant
  • inadeq recording of urine putput and stool pattern changes
  • mother and infant breast feeding complications***
  • short hospital stays
  • first time mothers
  • Tx: education!!!! supplemenetal feeding with pumped breast milk or formula for adequate hydration and reversal of hypovolemia if necessary
  • phototherapy if necessary
  • prevention!!
58
Q

Total serum bilirubin estimation with degree of caudal extension?

A
  • face: 5 mg/dL
  • upper chest: 10 mg/dL
  • abdomen: 12 mg/dL
  • palms and soles: greater than 15 mg/dL
59
Q

When should you suspect pathologic cause of jaundice?

A
  • if jaundice is seen in first 24 hrs (usually caused by hemolysis - medical emergency)
  • TB is greater than 95th percentile
  • rate of TB rise is greater than 0.2 mg/dL per hour
  • jaundice in newborn greater than 2 weeks of age
  • direct bilirubin greater than 1 mg/dL if TB is less than 5 mg/dL or more than 20% of TB is direct with TB greater than 5 mg/dL (suggests cholestasis)
60
Q

Common etiologies of unconjugated hyperbilirubinemia?

A

with hemolysis:

  • blood group incompatibility: ABO, Rh, Kell, duffy
  • sepsis
  • polycythemia

w/o hemolysis:

  • physiologic jaundice
  • human milk jaundice
  • breast milk jaundice
  • internal hemorrhage (cephalohematoma)
  • infant of diabetic mother
61
Q

What is SIDS? RFs?

A
  • unexplained death under 1 yo
  • peaks b/t 2-4 months
  • most occur in infants aged a few weeks to 6 months
  • RFs:
    sleeping position - belly
    bottle feeding
    maternal smoking (pre and postnatal)
    infant overheating
  • modifying risk factors:
    back to sleep and eliminate smoke exposure

Pediatrics (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions