Free RNC-NIC Exam Flashcards

A standardized tool combining 6 neuromuscular maturity signs (posture, square window, arm recoil, popliteal angle, scarf sign, heel-to-ear) and 6 physical maturity signs (skin, lanugo, plantar surface, breast, eye/ear, genitals) to estimate gestational age within about 2 weeks, even in extremely preterm infants.

Based on birth weight percentile for gestational age on a growth curve: SGA is below the 10th percentile, AGA is 10th-90th percentile, and LGA is above the 90th percentile. SGA infants have higher risk of hypoglycemia and polycythemia; LGA infants (often of diabetic mothers) have higher risk of hypoglycemia and birth trauma.

Early decelerations mirror contractions and reflect fetal head compression (benign). Late decelerations begin after the contraction peaks and reflect uteroplacental insufficiency (concerning for fetal hypoxia). Variable decelerations are abrupt and variable in shape/timing, reflecting umbilical cord compression.

A mnemonic for congenital infections that cross the placenta: Toxoplasmosis, Other (syphilis, varicella, parvovirus B19), Rubella, Cytomegalovirus, and Herpes simplex virus. Many share overlapping features - IUGR, hepatosplenomegaly, jaundice, thrombocytopenia, chorioretinitis, or microcephaly - so maternal history and specific serologies are needed to distinguish them.

PPV is started if the newborn is apneic or gasping, or if the heart rate remains below 100 bpm after the initial steps of warming, positioning, clearing the airway, drying, and stimulating.

Chest compressions begin if the heart rate stays below 60 bpm after 30 seconds of effective PPV with a secured airway and increased oxygen. Compressions and breaths are coordinated at a 3:1 ratio, delivering 90 compressions plus 30 breaths per minute.

IV or umbilical venous catheter (UVC) dosing is 0.01-0.03 mg/kg of the 1:10,000 (0.1 mg/mL) concentration, repeated every 3-5 minutes if the heart rate stays below 60. If only an ET tube is available while IV access is obtained, a higher ET dose of 0.05-0.1 mg/kg may be given, but the IV/UVC route is preferred because absorption is more reliable.

Normal saline (or O-negative blood if significant blood loss is suspected) is given at 10 mL/kg IV over 5-10 minutes for a newborn with signs of hypovolemia (pallor, weak pulses, poor perfusion) who is not responding to resuscitation.

The corrective step sequence used when PPV is not producing chest rise or improving heart rate: Mask adjustment, Reposition the airway, Suction the mouth and nose, Open the mouth, Pressure increase, and Alternative airway (ET tube or laryngeal mask).

Infants born extremely preterm are placed unwrapped and unwarmed into a polyethylene bag/wrap up to the neck immediately after birth and placed under a radiant warmer, since their thin skin and large surface-area-to-weight ratio make them prone to rapid evaporative heat loss.

Using commonly applied operational thresholds, treatment is indicated for a glucose below 40 mg/dL in the first 4 hours of life and below 45 mg/dL from 4-24 hours of life, since prolonged or severe hypoglycemia can cause neurologic injury.

Early-onset hypocalcemia occurs in the first 2-3 days of life, associated with prematurity, infant of a diabetic mother, or birth asphyxia, and is often asymptomatic or causes jitteriness. Late-onset hypocalcemia occurs after day 3, classically linked to high-phosphate formula/cow's milk intake or maternal vitamin D deficiency, and can present with tetany or seizures.

Small-volume feeds, roughly 10-20 mL/kg/day, given to preterm infants primarily to stimulate gut maturation, motility, and enzyme development rather than to meet full caloric needs; it is not advanced quickly and is often paired with parenteral nutrition.

Feeds are advanced gradually and held or reduced if feeding intolerance develops - increased gastric residuals, abdominal distension, or emesis - because rapid advancement is a recognized risk factor for necrotizing enterocolitis in this population.

The standard starting dose is 20 ppm, delivered through the ventilator circuit to selectively dilate the pulmonary vasculature and improve oxygenation in persistent pulmonary hypertension of the newborn (PPHN) without causing systemic hypotension.

Respiratory acidosis shows a low pH with an elevated PaCO2, reflecting a primary ventilation problem such as inadequate minute ventilation. Metabolic acidosis shows a low pH with a low bicarbonate, reflecting a primary problem with acid production or loss (e.g., poor perfusion, sepsis, NEC), often with a compensatory drop in PaCO2.

A respiratory pause of 20 seconds or longer, or a shorter pause accompanied by bradycardia (heart rate below 100 bpm) and/or desaturation, most commonly due to immaturity of the respiratory control center; first-line treatment is caffeine citrate.

Early CPAP or high-flow nasal cannula supports alveolar recruitment and reduces the work of breathing in preterm infants with respiratory distress syndrome, and is used preferentially over intubation and mechanical ventilation when possible to reduce ventilator-associated lung injury.

Conduction (direct contact with a cold surface), convection (cool air currents moving across the skin), evaporation (moisture evaporating from wet skin, greatest right after birth), and radiation (heat transfer to nearby cooler objects without direct contact, e.g., a cold incubator wall).

Cold stress triggers nonshivering thermogenesis through brown fat metabolism, which increases oxygen consumption and glucose use, and can lead to hypoglycemia, metabolic acidosis, increased pulmonary vascular resistance, and respiratory distress if not corrected.

Exogenous surfactant is instilled into the airway to reduce alveolar surface tension and prevent alveolar collapse in preterm infants with (or at risk for) respiratory distress syndrome; it is most effective when given early, and infants must be monitored for rapid improvement in lung compliance requiring prompt ventilator weaning.

Prostaglandin E1 (alprostadil/PGE1) is infused to keep the ductus arteriosus open in ductal-dependent congenital heart disease. Indomethacin, ibuprofen, or acetaminophen, which inhibit prostaglandin synthesis, are used instead to pharmacologically close a symptomatic patent ductus arteriosus.

A methylxanthine that stimulates the central respiratory drive and improves diaphragmatic contractility, reducing apnea/bradycardia episodes; early caffeine in very preterm infants is also associated with lower rates of bronchopulmonary dysplasia.

Skin-to-skin holding, combined with reducing ambient light and noise, supports autonomic and neurobehavioral stability and promotes parent-infant bonding; both are core elements of neuroprotective developmental care aimed at improving long-term outcomes for high-risk neonates.

Functional closure occurs within about the first 24 hours after birth, triggered mainly by rising arterial oxygen tension and falling circulating prostaglandin E2, which causes ductal smooth muscle constriction. Permanent anatomic closure through fibrosis follows over the next several weeks.

Ductal-dependent lesions need the ductus arteriosus to stay open for survival: ductal-dependent systemic flow (e.g., hypoplastic left heart syndrome, critical coarctation), ductal-dependent pulmonary flow (e.g., pulmonary/tricuspid atresia, severe tetralogy of Fallot), and ductal-dependent mixing (e.g., transposition of the great arteries). The '5 T's' cyanotic lesions are Tetralogy of Fallot, Transposition of the great arteries, Truncus arteriosus, Tricuspid atresia, and Total anomalous pulmonary venous return.

Failure of the normal drop in pulmonary vascular resistance after birth causes right-to-left shunting through the ductus arteriosus and/or foramen ovale, producing severe hypoxemia with a pre-/post-ductal oxygen saturation gap that is often out of proportion to chest X-ray findings.

Tachypnea, tachycardia, hepatomegaly, poor feeding or failure to thrive, diaphoresis with feeds, and a gallop rhythm; hepatomegaly is a particularly useful early sign of systemic venous congestion in infants.

Caused by surfactant deficiency in preterm lungs, leading to alveolar collapse, reduced compliance, and progressive respiratory failure. The classic chest X-ray shows a diffuse ground-glass pattern with air bronchograms; treatment is surfactant plus respiratory support.

Caused by delayed clearance of fetal lung fluid, more common after cesarean delivery (especially without labor) or precipitous delivery. Presents with tachypnea shortly after birth and typically resolves within 24-72 hours with supportive care alone.

Aspiration of meconium-stained amniotic fluid causes airway obstruction, chemical pneumonitis, and surfactant inactivation; chest X-ray shows patchy infiltrates with hyperinflation, and affected infants are at risk for secondary persistent pulmonary hypertension.

A chronic lung disease of prematurity defined by a continued need for supplemental oxygen at 28 days of life, with severity further graded by oxygen/respiratory support needs at 36 weeks postmenstrual age; it is driven by lung injury from prematurity, mechanical ventilation, and oxygen exposure.

Suspect with sudden clinical deterioration - desaturation, hypotension, asymmetric chest rise or breath sounds, and a shifted point of maximal cardiac impulse; a tension pneumothorax requires emergent needle decompression or chest tube placement.

An inflammatory bowel injury seen mainly in preterm infants, presenting with abdominal distension, feeding intolerance, and bloody stools. Pneumatosis intestinalis (gas within the bowel wall) on abdominal X-ray is the classic diagnostic finding; free air indicates perforation.

Gastroschisis is a defect lateral to a normally inserted umbilical cord with no covering sac, so bowel is exposed directly to amniotic fluid, and it has few associated anomalies. Omphalocele is a defect at the umbilical ring covered by a peritoneal sac, with the cord inserting into the sac, and is frequently associated with other congenital anomalies or syndromes.

Bilious emesis is a surgical emergency until proven otherwise. A 'double bubble' sign on abdominal X-ray suggests duodenal atresia, while sudden bilious vomiting with a distended, tender abdomen raises concern for malrotation with volvulus requiring urgent surgery.

Absence of ganglion cells in a segment of distal colon prevents normal peristalsis, classically presenting as failure to pass meconium within the first 24-48 hours of life, abdominal distension, and bilious vomiting; diagnosis is confirmed by rectal biopsy.

Physiologic jaundice appears after 24 hours of age, typically peaking around day 3-5 in term infants, from increased bilirubin production combined with immature hepatic conjugation. Jaundice appearing within the first 24 hours of life is always pathologic and requires prompt evaluation for hemolysis, infection, or other causes.

The Bhutani nomogram plots an hour-specific total bilirubin on a percentile curve to predict the risk of significant hyperbilirubinemia and guide follow-up and phototherapy timing. Untreated severe hyperbilirubinemia can cause kernicterus - bilirubin deposition in the basal ganglia causing lethargy and hypotonia progressing to hypertonia, with long-term risk of choreoathetoid cerebral palsy and hearing loss.

A positive direct Coombs test detects antibody-coated red blood cells and supports a diagnosis of hemolytic disease of the newborn (Rh or ABO incompatibility) as the cause of early or rapidly rising bilirubin, distinguishing it from non-hemolytic causes.

Defined as a central venous hematocrit above 65%, since capillary heel-stick samples can read falsely high. Risk factors include IUGR/SGA, delayed cord clamping, and infant of a diabetic mother; hyperviscosity can cause hypoglycemia, respiratory distress, and poor perfusion.

Bleeding from the fragile germinal matrix, most common in infants born before about 32 weeks or under 1500 g, usually within the first 72 hours of life. Graded I-IV by extent (subependymal, intraventricular without dilation, intraventricular with ventricular dilation, and parenchymal extension).

Ischemic injury to the white matter surrounding the lateral ventricles in preterm infants, seen as cystic changes on cranial ultrasound or MRI, and strongly associated with later cerebral palsy (especially spastic diplegia) and cognitive impairment.

Brain injury from perinatal asphyxia, staged using Sarnat staging (mild, moderate, or severe based on consciousness, tone, reflexes, seizures, and autonomic function). Therapeutic hypothermia to about 33.5°C, started within 6 hours of birth, is standard treatment for moderate-to-severe HIE to reduce death or disability.

Early-onset GBS disease occurs within the first 7 days of life, most within 24-48 hours, from vertical transmission during labor and delivery, and is reduced by intrapartum antibiotic prophylaxis for GBS-colonized mothers. Late-onset GBS disease occurs from 7 days to about 3 months of age, is not prevented by intrapartum prophylaxis, and more often presents as meningitis or bacteremia.

Because neonates cannot localize infection, sepsis often presents with subtle findings: temperature instability (hypo- or hyperthermia), lethargy, poor feeding, apnea or bradycardia, and respiratory distress - any of which should prompt a sepsis evaluation in a high-risk infant.

An approach that treats parents as active partners in their infant's care - through open communication, involvement in rounds and care decisions, unrestricted presence, and education - which has been shown to reduce parental stress and improve infant outcomes.

Nurses should use the infant's name, offer options such as holding the infant and creating memory items like photos or hand/footprints, avoid euphemisms that minimize the loss, and connect families with bereavement or chaplaincy support and follow-up resources.

Because neonates cannot consent for themselves, parents or legal guardians provide informed permission for procedures after being given the risks, benefits, and alternatives in understandable terms; the nurse's role includes verifying understanding and advocating for the family in decision-making.

NICU teams use standardized care bundles built from current research evidence - such as central-line maintenance bundles to reduce CLABSI and skin-care protocols to reduce pressure injury - and track outcome data to drive continuous quality improvement.