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25 Cards in this Set
- Front
- Back
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Congenital abnormalities |
Mental or physical, may be present at birth or diagnosed later, limbs/organs may be malformed, duplicated or absent, |
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Form of congenital abnormalities |
Result from abnormal gene residing on one of 22 pairs of autosomal chromosomes, can be dominant or recessive |
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Prenatal diagnosis |
Amniocentesis Ultrasound |
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Amniocentesis |
Take amniotic fluid b/t 15-18 weeks of pregnancy, test cells for abnormalities |
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Ultrasound |
Identify spine and skull abnormalities in early pregnancy |
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Conjoined twins |
Results when separation process of identical twins fail, may be separated depending on site of pagus |
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Prematurity |
Birth before 37 weeks gestation, low weight, leading cause of death in neonatal period, incomplete development of organ system |
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Prematurity symptoms and signs |
Little subcutaneous fat, palms and soles with few creases, Undescended make testes, prominent female clitoris Lack ability to suck/swallow, underdeveloped lungs, immature neurologic system |
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Etiology of prematurity |
Incomplete cervix, bicornate uterus, toxic conditions, maternal infection, trauma, premature rupture or amniotic membrane, intrauterine fetal growth retardation |
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Treatment of prematurity |
Iv fluids and hyperalimentation to encourage growth and development, airway management and pulmonary functioning monitored, monitor O2 saturation, heart rate, and body temp |
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Prematurity prognosis |
Varies depending on gestational age/weight, and abnormalities. Risks: cerebral bleed, underdeveloped pulmonary system. Accepted gestational age: 24wks |
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Infant respiratory distress syndrome (IRDS) |
Signs: nasal flaring, grunting respiration and sternal retractions, become cyanotic |
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IRDS Etiology |
Lungs of neonate lack surfactant needed to allow alveoli to expand, reduced potential for adequate gas exchange |
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IRDS treatment |
Treatment: administration of carefully titrated supplemental oxygen, aerosol infusion of surfactant allows alveoli to expand Prevention is best treatment |
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Laryngomalacia, tracheomalacia, bronchomalacia |
Can be separate or combination, primary cause is softened or underdeveloped cartilage allowing airway structure to collapse. Sign/symptoms: respiratory strider, dyspnea, cyanosis |
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Bronchopulmonary dysplasia (BPD) |
Lungs are stiff, obstructed, hard to ventilate, infant experiences periods of dyspnea, including tachypnea, wheezing, cyanosis, nasal flaring, and sternal retraction, coughing, difficulty feeding. Occurs in many premature infants after IRDS mechanical ventilation w/supplemental O2, and infection or pneumonia Goal of treatment is to replace damaged alveoli |
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Retinopathy of prematurity (ROP) |
Occurs most w/ infants born before 28 weeks, no visible symptoms, vascularization of retina begins at central part of eye as vessels grow out. Incomplete vascularization of retina. No risk factors, high supplemental O2 often responsible, or certain drugs for immature lungs. Mild forms resolve w/o treatment |
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Necrotizing enterocolitis (NEC) Symptoms |
Develop after birth Feeding intolerance, abdominal distention, bile colored emesis, diarrhea, tender abdomen, blood in stool, decreased or absent bowel sounds, lethargy, temp instability |
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NEC Etiology |
Unknown, believed to be breakdown of normal defense system in GI tract Blood and stool cultures preformed |
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NEC treatment |
Aggressive and immediate intervention necessary. Feeding stopped, tube inserted into stomach, fluids and antibiotics administered through IV, respiratory and pH monitored by arterial blood gasses. Weight, intake, output, and abdomen monitored |
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Robinow syndrome |
Dominant or recessive forms, mild to moderate characteristics, normal intelligence but have physical development issues Genetic syndrome, responsible gene not established Treatment: address treatable condition: dental abnormalities, cleft palate, scoliosis, genetic or psychosocial counseling recommended |
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Cri-du-chat syndrome (cats cry) |
Deleted genetic material from chromosome 5. Results in stillborn child or death soon after. Microcephaly w/brain tissue deficiency. Surviving children:slow growth, small head, poor muscle tone, mental retardation No cure |
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Hypertrophic cardiomyopathy |
Major cause of sudden death in young athletes. First sign is collapse of seemingly healthy athlete. Symptoms: chest pain, syncope, hypertension, palpitations, shortness of breath Diagnosis made on autopsy ECG or MRI may indicate hypertrophy Meds: beta blockers and calcium channel blockers |
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Down’s syndrome |
Associated w/heart defects and other congenital abnormalities. Infant has small heads/flat back skull, slant to the eyes, flat nasal bridge, small low set ears, small mouth w/protruding tongue, small weak muscles Extra chromosome #21 |
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Treatment for Down syndrome |
Care depends on severity of physical defects and mental impairment Treatment plan is individual and includes a multidimensional approach to maximize the development of motor and mental skills |
