25.3: Congenital, Genetic, and Acquired Complications
By the end of this section, you will be able to:
- Identify and define common congenital and genetic disorders found in the newborn
- Describe the nursing management of newborns with common congenital and genetic disorders
- Describe characteristics, common medical conditions associated with, and therapeutic management of genetic diseases, including both phenotype and environmental modification
- Discuss the nurse’s role in educating, caring for, and supporting families and newborns with congenital and genetic disorders or conditions
A congenital disorder is a disorder or abnormality present at birth, while a genetic disorder is caused by an abnormality in the genetic material, chromosomes, or the genes within the chromosomes (Udayangani, 2022).
Support of the family during the introduction of the newborn with a congenital or genetic disorder is paramount. These disorders can be known or unknown at the time of birth and can make attachment and bonding difficult. The role of the nurse is to support the birth parent and newborn during this time of transition while also facilitating bonding and attachment.
Cranial and Craniofacial Deformities
A cranial deformity is a congenital or genetic disorder that affects the development of the cranial anatomy resulting in abnormal form or function. The disorders that fall under this category can be noted in utero or at birth. They are usually diagnosed very early in life because of visually notable facial features and potentially measurable size differences.
Microcephaly
One cranial deformity is microcephaly , which is a head circumference at least two standard deviations below the average findings for someone of the same age and gender (The National Center on Birth Defects and Developmental Disabilities [NCBDDD], n.d.). Microcephaly can be a finding and diagnosis, or it can be a finding related to an underlying disorder or disease pattern. Microcephaly can be connected to comorbid disorders including seizures, developmental delay, intellectual disabilities, hearing or vision loss, movement and/or balance problems, and feeding difficulties, particularly swallowing (Harris, 2015).
Craniosynostosis
Craniosynostosis is defined as two or more prematurely fused skull bones. There is a range of presentations, but the most common type presents with the closure of one suture in the skull earlier than expected. The disease can affect multiple skull bones or even bones outside the cranium.
Craniosynostosis can be a cosmetic deformity, but the more concerning result is that it can potentially limit brain growth and development. Growth of the brain relies on skull growth to allow for internal expansion. Surgical correction is required to allow appropriate brain growth if sutures are not present for movement during growth. The potential neurocognitive impact of craniosynostosis is just now being investigated by the research community (Proctor & Meara, 2019).
Cleft Lip and Cleft Palate
A cleft is a congenital abnormal space or gap in the upper lip, alveolus, or palate. A cleft lip or cleft palate can occur alone or can be found together as a cleft lip and palate. A cleft lip is a failure of the tissues to come together at the frontonasal and maxillary processes. A complete cleft lip has a gap that extends through the nasal floor; an incomplete cleft does not. A cleft palate occurs when the palatal shelves that make up the maxillary processes do not come together. The way these defects present is determined by when in embryologic life the interference in fusion occurs (Vyas et al., 2020) (Figure 25.5).
Etiology
Cleft lip and cleft palate can occur as lone congenital defects or with other congenital defects, specifically with congenital heart disease . Both are associated with more than 300 diagnosable syndromes (Vyas et al., 2020).
Cleft lip and cleft palate occur in approximately 1 in 600 to 800 live births (1.42 in 1,000), while the less common cleft palate alone occurs in around 1 in 2,000 births. These defects are distributed as follows: 15 percent are cleft lip alone, 45 percent are cleft lip and palate, and 40 percent are cleft palate alone (Shankar, 2011).
Pathophysiology
It is believed that cleft lip and cleft palate occur as result of a combination of genetic and environmental factors. These conditions can lead to difficulty in feeding by bottle or breast, which increases the risk of developmental delay and slowed growth. Children with these defects can experience difficulties in speech development, deafness, malocclusions, notable facial deformation, and potentially severe psychologic issues (Vyas et al., 2020).
Diagnostics
Diagnosis of cleft lip, cleft palate, or cleft lip and palate usually occurs by ultrasound before birth. Early detection allows for early education for the parents and early intervention to alleviate any difficulties with feeding. Parents who do not have access to prenatal care learn about their child’s cleft only after birth.
Cleft Lip and Palate: The View from Those Practicing Hinduism
Beliefs and attitudes of people play a major role in how they perceive and respond to any physical deformity. Cultural views and opinions based on those cultural beliefs have a role in how the family views their child with the physical deformity. Families who practice Hinduism, a dominant religion of India that is characterized by a belief in reincarnation, may believe that cleft lip and/or cleft palate are the result of sins from a past life visiting the newborn in this life or some other supernatural cause (Weatherly-White et al., 2005).
Nursing Management
It is very important to treat clefts at the right time or right age to get the most effective repair with as little impairment as possible (Vyas et al., 2020). The long-term management of a cleft lip and cleft palate requires a multidisciplinary team: plastic surgery, otolaryngology, orthodontics, speech pathology, pediatrics, nursing, audiology, social work, and psychology. Surgical correction and successful reconstruction typically require multiple stages or phases of surgery (Vyas et al., 2020).
Nursing management of an infant with cleft lip and palate begins with assessment of the family as a whole. The nurse explores the family’s understanding and acceptance of its new member and asks how feeding is being done. The nurse determines by physical assessment during feeding if effective nutritional intake is occurring and evaluates growth over time. The goals of caring for this newborn include maintaining hydration and nutrition and reducing the parents’ potential anxiety and guilt that may occur related to the newborn’s physical defects.
Educating the caregiver on how to feed a newborn with cleft palate is a vital role of the nurse. Direct breast-feeding can be successful, as the breast tissue itself can fill the gap in the lip and/or palate. When using a nipple to feed a newborn with cleft lip and palate, positioning in a unilateral presentation can improve intake. The person feeding the infant should aim the nipple at the unaffected side of the palate. An extra-long nipple, such as that used on the Haberman feeder (Figure 25.6), Lamb’s nipples, and/or special cleft palate nipples can be used to close the opening in the palate. An Asepto syringe with the addition of rubber tubing on the tip, also called a Breck feeder, can be successful for feedings (National Health Service [NHS], 2023).
Fetal Alcohol Spectrum Disorders
Fetal alcohol spectrum disorders (FASD) are the potential outcome of prenatal alcohol exposure (PAE) combined with genetic and environmental factors (Kaminen-Ahola, 2020). Effects of the disorder can range from growth deficits to physical abnormalities, neurocognitive and behavioral deficits, and an increased vulnerability to mental health problems later in life.
The five major diagnoses of FASD are based on the particular symptoms displayed:
- Alcohol-related neurodevelopmental disorder—defined as a disorder with intellectual disabilities or behavioral and/or learning problems caused by maternal alcohol consumption during pregnancy
- Alcohol-related birth defects—a range of congenital and genetic birth defects caused by maternal alcohol consumption during pregnancy
- Fetal alcohol syndrome —fetal alcohol spectrum disorder at its most severe presentation, including both neurodevelopmental disorders and congenital and genetic birth defects caused by maternal alcohol consumption during pregnancy
- Partial fetal alcohol syndrome—some, but not all, the hallmark signs and symptoms of fetal alcohol syndrome caused by maternal alcohol consumption during pregnancy; ultimately the criteria for the diagnosis of FAS are not met
- Neurobehavioral disorder associated with prenatal alcohol exposure—behavioral symptoms of a disorder that include neurocognitive impairments such as problems with mental health, long- and short-term memory, impulse control, communication, and daily living activities; caused by maternal alcohol consumption during pregnancy (Mayo Foundation for Medical Education and Research [MFMER], 2018)
Fetal alcohol syndrome is the most severe of these disorders. This diagnosis includes characteristic facial dysmorphisms and central nervous system deficits.
Etiology
Many factors affect the developmental and health status of the infant with FASD: genetic susceptibility, the pregnant person’s drinking pattern, the timing of drinking in relationship to what fetal development takes place at that time, and the amount of alcohol consumed, along with the pregnant person’s metabolism and tolerance of alcohol during the pregnancy. FASD prevalence ranges from 3 percent to 5 percent in Europe and North America to more than 10 percent in South Africa, although this disorder is underdiagnosed (Kaminen-Ahola, 2020).
Pathophysiology
Recent research findings suggest that PAE may affect the regulation of gene expression. Epigenetic regulation and the variation induced in utero from the teratogen alcohol could be the underlying pathophysiology of FASD. Drinking alcohol while pregnant allows alcohol to enter the bloodstream and reach the fetus via the placenta. The developing fetus experiences higher concentrations of alcohol than the pregnant person because the fetus metabolizes alcohol more slowly than an adult. Alcohol can then affect all developing tissues and interfere with oxygen delivery and nutritional intake. The more alcohol that is ingested, the greater the risk to the fetus as it develops (MFMER, 1998–2023). The major signs and symptoms of FAS include the following:
-
Three specific facial abnormalities:
- smooth philtrum (the area between nose and upper lip)
- thin upper lip
- small palpebral fissures (the horizontal eye openings)
- Growth deficit (lower than average height, weight, or both)
- Central nervous system (CNS) abnormalities (structural, neurologic, functional, or a combination of these) (American Academy of Pediatrics [AAP], 2018)
Diagnostics
Diagnosing FAS requires a multidisciplinary team including the primary pediatrician, a geneticist, and a neuropsychologist. Chromosomal testing can be a piece of diagnostics, but only 9 percent to 14 percent of children diagnosed with FASD will have chromosomal deletions or duplications directly causative of the child’s features. Currently, research is focused on finding biomarkers that could be used for simple blood tests to diagnose the disorder (Kaminen-Ahola, 2020).
Nursing Management
No specific treatment for FASD exists, but the earlier it is diagnosed, the sooner supportive services can be added to the child’s life. The physical and mental deficiencies of FASD will be ongoing, requiring a lifetime of coordinated medical care and support. The nurse assists with contacting social services if the birthing institution allows or consulting child protective services (CPS) with any newborn diagnosed with FAS. In many states in the United States, children born with FASD are automatically immediately eligible for intervention services.
The goal of treatment is to reduce the effects of the syndrome and prevent as many disabilities as possible. Early intervention services—speech therapy, physical therapy, and occupational therapy—can reduce FAS effects and prevent some long-term disabilities. Developmental services include consultation with an early interventionist and help with basic gross motor and social skills. Later childhood care can include a psychologist along with supportive services in school to help with learning and behavioral issues. Every child presenting with FASD has their own personalized needs. This individualized care may include optometry for vision care or a cardiologist for cardiovascular health, for example, though other children with FASD may not need these specific medical specialists.
Nursing management includes assessment for overstimulation because infants with FAS can become agitated easily and have difficulty self-soothing. Maintaining an environment that is calm and stable by clustering care decreases physical stimulation. The family and/or pregnant person will need to be assessed for alcohol and other substance-use problems. The nurse educates the birth parent that no amount of alcohol during pregnancy is safe for a fetus. If the infant has siblings, they also may need to be evaluated for the disorder. The nurse provides education to the birth parent along with counseling that includes alcohol cessation programs and support groups. Because FASD is a lifelong disorder that affects not only the infant but also the whole family, counseling can benefit parents and the family in dealing with their child's physical and behavioral problems.
Genetic Disorders
Genetic disorders are an inherited medical condition caused by a change in the DNA. The effects of the DNA abnormality can range from encompassing multisystemic disease states to benign disease states that rarely cause significant life changes. The most significant genetic disorders are those that cause life-altering medical conditions that affect the patient from birth throughout their life.
Trisomy 21
Down syndrome (DS) , or Trisomy 21 , is the most commonly occurring chromosomal anomaly. It is primarily caused by trisomy of chromosome 21, which results in the multisystem signs and symptoms of the syndrome. Langdon Down first described the condition in 1866 in a paper presented at a lecture conference (Down, 1887). Many care providers had come to the conclusion that there was a genetic basis long before testing, developed in 1959, could confirm that Down syndrome was caused by a chromosomal anomaly (Antonarakis et al., 2020).
Etiology
Down syndrome (DS) is the most common genetic disorder of intellectual disability. The prevalence is increasing as the global population grows, while more children with DS survive childhood. Trisomy 21 occurs in about 1 in 700 to 800 births (6.7 in 10,000) or 1 in 779 infants born in the United States (Antonarakis et al., 2020). Elective termination or spontaneous abortion of fetuses with DS results in a reduction of the final number of live infants born with the finding.
Pathophysiology
Molecular pathophysiology research currently suggests that DS is a disorder of gene expression dysregulation. However, further research is needed. The biological mechanism that results in each type of phenotypic presentation remains unknown. Different types of meiotic and mitotic errors can all lead to aneuploidy and, ultimately, trisomies.
Advanced maternal age (AMA) at conception is a major risk factor for DS and is a risk factor for all autosomal trisomies. However, most newborns with trisomy 21 are born to those who are not AMA, due to the number of live births within that age group. Environmental factors are also influential in this disorder, among them tobacco use, lack of folic acid supplementation, and oral contraceptive use (Antonarakis et al., 2020).
Diagnostics
Laboratory-based prenatal screening for DS is offered as routine antenatal care in developed countries. The serum sample for screening measures maternal levels of beta human chorionic gonadotropin and other gestationally age-dependent levels. First trimester ultrasound is used to measure fetal nuchal translucency. No one specific fetal anatomic finding is diagnostic of DS; rather, there are so-called soft signs associated with the syndrome. Best practice guidelines recommend that if any of these early testing methods is positive, the pregnant person should be offered posttest counseling and a diagnostic test: amniocentesis or chorionic villus sampling , followed by a genetic analysis (Antonarakis et al., 2020).
Nursing Management
Every person with DS has their own strengths and challenges related to their health that will vary throughout their life. The level of medical care required from birth can be high or low, depending on the comorbidities. This same presentation is paralleled as children with DS age. Some may need multiple layers of social care and support while others may live independently. Some health problems have a higher incidence in those with DS: congenital heart disease , obstructive sleep apnea, thyroid disease, dementia, epilepsy, gastrointestinal disease, hearing and vision problems, intellectual and developmental disabilities, mental illness, immunologic dysfunction, hematologic disorders, and musculoskeletal issues (Alexander et al., 2015). The American Academy of Pediatrics (AAP) has screening guidelines to address these potential areas of care (Bull et al., 2022), including a recommendation to have an evaluation by a cardiologist for a cardiac baseline early in the infant period.
Trisomy 18 and Trisomy 13 Syndromes
Trisomy 18 , or Edwards syndrome , and Trisomy 13 are genetically and phenotypically distinct diseases. However, they have very similar characteristics and survival rates, and they rely on much the same treatment and management (Carey et al., 2021). Edwards syndrome is named after Professor John Edwards, who originally described the syndrome in a 1960 issue of The Lancet , the same edition where Patau described the syndrome of trisomy 13 (Edwards et al., 1960; Patau et al., 1960).
Incidence
The incidence of trisomy 18 ranges from 1 in 3,600 to 1 in 8,500 live births (Carey et al., 2021). The incidence of trisomy 13 is estimated to range from 1 in 5,000 to 1 in 12,000 total births (Carey et al., 2021). These pregnancies many times end in spontaneous miscarriage without diagnosis (Carey et al., 2021).
Etiology and Pathophysiology
Trisomy 18 includes a recognizable constellation of major and minor findings, most notably increased neonatal and infant mortality and significant developmental and motor disabilities for children who survive past infancy. Most infants with trisomy 18 have a full three copies of chromosome 18 in all their cells. A small percentage, 3 percent to 6 percent of infants with this disorder, have mosaicism, or partial presentation, of the chromosomal trisomy. The addition of an extra chromosome in trisomy 18 was found to be maternal nondisjunction in 95 percent of the studied cases. Nondisjunction occurs when chromosomes fail to segregate during meiosis; when this happens, gametes with an abnormal number of chromosomes are produced, leading to pregnancy loss or birth defects. As in all trisomies, the occurrence of nondisjunctional trisomy 18 increases with advanced maternal age (Carey et al., 2021).
Trisomy 13 syndrome presents as a pattern of multiple congenital anomalies including a combination of orofacial clefts, micro- or anophthalmia, and postaxial polydactyly, which is easily identified and diagnosed on presentation (Carey et al., 2021). Table 25.3 compares trisomy 18 and 13 features.
| Syndrome | Features |
|---|---|
| Trisomy 18 |
|
| Trisomy 13 |
|
Diagnostics
Both disorders have a characteristic pattern of prenatal growth deficiency. Trisomy 18 presents with distinctive craniofacial features, hand posturing with overriding fingers and small nails, and a short sternum. These can be enough for a clinical diagnosis of the disease in utero, but confirmation of the syndrome requires a standard G-banded karyotype or, more recently, a cytogenomic single nucleotide polymorphism (SNP) microarray that shows the extra copy of chromosome 18 (Carey et al., 2021).
Trisomy 13 presents with orofacial clefts, micro- or anophthalmia, and postaxial polydactyly. However, any newborn with holoprosencephaly and multiple anomalies should be considered for the syndrome. Ear malformations, anterior frontal upsweep, and capillary malformations of the forehead are common enough in the syndrome to be helpful in determining a clinical diagnosis. Any clinical diagnosis of trisomy 13 needs to be confirmed with a SNP microarray or karyotype that shows three full copies of chromosome 13 or most of the long arm of chromosome 13. Maternal nondisjunction is the most common reason for the trisomy, accounting for approximately 90 percent of cases. However, mosaicism and translocation can also be the underlying cause for the extra genetic material (Carey et al., 2021).
Nursing Management
Both trisomy 18 and 13 result in anomalies that, without intervention and sometimes even with it, lead to death in the first months of life. Both are common disease processes present in miscarried zygotes or fetuses. Around 50 percent of newborns with trisomy 18 or 13 survive for longer than a week after birth, and 6 percent to 12 percent of those will live beyond a year (Carey et al., 2021).
Recently, the health-care community has changed the management paradigm for infants with trisomy 18 and 13. When parents choose to proceed with full intervention instead of comfort or palliative care only, pediatric otolaryngology and pediatric cardiology become involved in a multidisciplinary approach to care. The most likely driving factors in the interventional care of the patient with either trisomy 18 or 13 are respiratory (airway) and cardiac (congenital cardiac disorder) that will be treated early in life (Carey, 2021; Carey et al., 2021).
Turner Syndrome
Turner syndrome (TS) is a genetic disorder where phenotypic females have one X chromosome and complete or partial absence of the other sex chromosome. The syndrome is associated with typical clinical signs and/or symptoms that can include short stature, hypergonadotropic hypogonadism, infertility, middle ear infection, and other congenital malformations. In the newborn, the classic assessment findings are webbed neck, low birth weight, and congenital cardiac disease, most likely aortic arch related. The syndrome was first described by Henry H. Turner in a journal publication in 1938, but the disease pattern was previously described by Giovanni Battista Morgagni in 1768 and N. A. Shereshevski in 1930 (Gravholt et al., 2022).
Etiology
Understanding of the genetics and genomics of TS is currently evolving as new information emerges from active research. New studies show “pervasive changes in methylation pattern and RNA expression” (Gravholt et al., 2022). New candidate genes for phenotypic expression and genotypic traits have emerged, although more research is needed in this area. The estimated prevalence of TS in newborns is approximately 64 per 100,000 (Gravholt et al., 2022); however, the number in the general population of adult women is significantly lower due to missed diagnosis and mortality. The average age of diagnosis is 15 years, but with newborn screening and cord blood testing, neonatal diagnosis is increasing (Gravholt et al., 2022).
Pathophysiology
Infants with TS will have some, though likely not all, features noted at birth. Other general features will emerge throughout their lifetime, some found in more cases than others. Table 25.4 lists the features of Turner syndrome.
| Type of Features | Features |
|---|---|
| At birth |
|
| General |
|
Most instances of TS are not inherited (Gravholt et al., 2022). Monosomy X is a random formation of reproductive cells in the parent of the person with TS. An error in cell division can result in reproductive cells with an abnormal number of chromosomes, in this case one less. If an atypical reproductive cell is a part of the genetic makeup of a zygote, each cell will possess a single X chromosome. The other sex chromosome will be missing, as it was missing in the original atypical cell. Mosaic Turner syndrome is also not an inherited condition. It occurs because of a random event during cell division in early fetal development. Mosaic TS results in some cells having the usual number of chromosomes and some cells having only one sex chromosome. In rare instances, TS can be from a partial deletion of the X chromosome, and this can pass from one generation to the next, the only inheritable form of the syndrome (Kikkeri & Nagalli, 2022).
Diagnostics
The diagnosis of TS relies on both the clinical phenotype and a standard chromosomal analysis.  It is recommended that all infants diagnosed prenatally have a postnatal karyotype to confirm the diagnosis (Gravholt et al., 2017). The most common karyotype of TS is 45, X (40 percent to 50 percent). The mosaic karyotype 45, X/46, XX is found in 15 percent to 25 percent of cases (Gravholt et al., 2017; Gravholt et al., 2022).
Nursing Management
Care of a newborn with TS will require an interdisciplinary team. Fifty percent of children with TS will have congenital heart disease, and almost all will have an underlying endocrinologic disease, with decreased growth and a high incidence of diabetes (Gravholt et al., 2017). After diagnosis of TS, an infant will need the care of a general pediatrician as well as a pediatric endocrinologist who may start therapy as early as 1 year of age to increase linear growth. A pediatric cardiologist should be consulted to monitor for aortic changes and to evaluate for prolonged QT intervals and the presentation of hypertension. A geneticist may be needed to counsel the family and delineate the specific genotype (Gravholt et al., 2017).
All newborns with suspected genetic disorders benefit from early diagnosis together with a team or developmental home where their care is coordinated by many different professionals and services, such as neonatologists, clinical geneticists, social workers, and developmental specialists along with needed therapies.
The National Institutes of Health provides extensive information on genetic and rare diseases at the Genetic and Rare Diseases Information Center.
Congenital Heart Disease in the Newborn
Congenital heart disease (CHD) affects 0.6 percent to 1.9 percent of live births every year in the United States (Desai et al., 2023). Congenital cardiac defects can be divided into cyanotic lesions, those defects that shunt right to left (patients who have oxygen saturations less than 90 percent), and acyanotic lesions, defects that shunt left to right (expected oxygen saturations, 90 percent and above). Both cyanotic and acyanotic congenital cardiac defects can be divided again into increased pulmonary blood flow, decreased pulmonary blood flow, obstructed blood flow, and mixed lesions. Cyanotic heart defects are those that provide less than normal oxygenated blood to systemic circulation, resulting in a lowered oxygen saturation at baseline. These defects have an incidence of approximately 57 in 100,000 births (Sadowski, 2009). Congenital heart disease is one of the most common birth anomalies affecting neonates and one of the most survivable because palliative surgical options and medical management have improved significantly over the past few decades.
Ductal-dependent lesions depend on a patent ductus arteriosus to provide systemic blood flow. Examples of ductal-dependent defects are hypoplastic left heart syndrome (HLHS), coarctation of the aorta, interrupted aortic arch, critical aortic stenosis (AS), pulmonary stenosis (PS), pulmonary atresia with intact ventricular septum (PAIVS), tricuspid atresia (TA), and transposition of the great vessels (TGV).
Figure 25.7 illustrates congenital heart disease types grouped by category (Sadowski, 2009).
Risk Factors
Risk factors for CHD can be broken down into six categories. Prematurity increases the incidence to 2 to 3 times that of a term newborn. Family history of a first-degree relative having a CHD is 3 to 4 times that of the general population. Left-sided obstructive lesions have a much higher recurrence risk in families. Genetic syndromes and other extracardiac congenital defects are commonly found in the CHD population. Chromosomal defects were found in 7 percent of patients who had CHD. Certain maternal conditions increase the risk of CHD in the fetus: obesity, type 1 or 2 diabetes mellitus, hypertension, phenylketonuria (PKU), thyroid disorders (hypothyroidism or hyperthyroidism), systemic connective tissue disorders (e.g., rheumatoid arthritis or lupus), and epilepsy (due to the anti-seizure medications used for seizure suppression). Maternal exposure to alcohol, smoking, phenytoin, and retinoic acid also increases the risk to the fetus. Assisted reproductive technology has also been linked to an increased risk of CHD, specifically septal defects (Altman, 2022). Congenital infections including maternal influenza and congenital rubella are also risk factors (Oster et al., 2011).
The most common congenital cardiac defect is the ventricular septal defect (VSD) . One out of every four cardiac defects is a VSD or includes a VSD in its defects. A murmur is the most likely finding at the first pediatrician visit within the first few weeks of life that leads to a diagnosis of VSD. Not all VSDs require surgical repair, and not all VSDs present in the same way. Some are multiple holes between the ventricular septal wall, while others are a single large opening in the ventricular septal wall (Figure 25.8). Note that the murmur (the sound that is heard where turbulent blood flow occurs through the defect) will be louder, the smaller the opening.
Pathophysiology
Congenital heart defects (CHD) occur in one in four live births and are among the most common congenital defects (see Figure 25.7). The structure and function of the heart and blood vessels are affected to varying degrees. Some conditions require very mild management and treatment. Others are life threatening and require staged palliative surgeries or a heart transplant (NCBDDD, 2022; Centers for Disease Control and Prevention [CDC], n.d.).
Diagnostics
Prenatal screening with fetal ultrasound has increased the prenatal diagnosis of CHD to 50 percent to 60 percent. With the addition of initial screening for CHD done in the newborn nursery with a pulse oximetry test, most infants with a CHD are diagnosed prior to release from in-hospital care, or discharge. However, some diagnoses, due to their PDA dependence and timing of screening, are not found prior to discharge (Altman, 2022). Increased pulmonary blood flow leads to the signs and symptoms of tachypnea, retractions, nasal flaring, and tachycardia, with the ultimate concerns for respiratory distress or failure.
Nursing Management
The type of defect determines what constitutes appropriate management. Most CHDs require palliative surgery. Surgical repair does not occur because the heart itself is never repaired but can only be palliated for the best outcome. For example, the size or placement of a VSD can allow for monitoring to see if the hole closes over time rather than surgically closing the hole during the neonatal period. Some critical congenital heart defects require multiple staged surgeries throughout the patient’s first years of life. Postoperative care is managed in an intensive care unit, either a neonatal intensive care unit or a cardiothoracic intensive care unit.
Congenital Defects of the Gastrointestinal and Genitourinary Systems
An esophageal atresia (EA) , also called a tracheoesophageal fistula (TEF) , is a fetal development anomaly in which the esophagus connects to the trachea (Figure 25.9). It is relatively common, occurring in 1 in 3,000 births. EA can be found as a solitary defect or can be associated with other midline defects such as congenital cardiac defects. It is also found in syndromes, most notably VACTERL syndrome, each letter of the anachronym standing for vertebral defects, anal atresia, cardiac defects, tracheoesophageal fistula, renal anomalies. and limb abnormalities (Oermann, 2022; Slater & Rothenberg, 2016).
Etiology
A TEF or an EA is caused by an error in fetal development of the lateral septation in the foregut that becomes the esophagus and trachea. The fistula tract that connects the esophagus and the trachea is thought to form a branch of the embryonic lung that does not continue to develop because of defective epithelial-mesenchymal interactions (Oermann, 2022).
Pathophysiology
The connection between the trachea and esophagus can lead to an excessive amount of air in the stomach, depending on where the connection arises and where the fistula occurs between the two organs, esophagus and trachea. The infant is unable to feed without aspirating oral liquids crossing from the esophagus to the trachea and subsequently into the lungs.
Diagnostics
The most common signs and symptoms of this disorder are the three C’s—coughing, choking, and cyanosis—particularly exhibited during feeding. Esophageal atresia, in which the esophagus ends before reaching the stomach, can be diagnosed by attempting to pass an oral or nasal catheter into the stomach and not being able to reach the gut. With the catheter in, chest and abdominal x-ray images confirm the shortened esophagus. A distal TEF is diagnostically confirmed with both an anterior-posterior and lateral chest x-ray showing a fully gas-filled stomach and intestines. A proximal TEF can be diagnostically confirmed with a fluoroscopic study using a small amount of water-soluble contrast. Barium should not be used because of the risk for aspiration and subsequent pneumonitis (Oermann, 2022). For more difficult TEF positioning, diagnosis includes an upper gastrointestinal series with water-soluble contrast. If the diagnosis is still unclear, a CT scan with airway reconstruction can clarify the anatomy of the airway (Oermann, 2022).
Nursing Management
Surgery to disconnect the trachea and esophagus or to connect the atretic esophagus to the stomach is the treatment. Preoperatively, the neonate would be NPO with no oral or gastric feeds or medications. Their nutrition would be provided by intravenous methods with partial or total parenteral nutrition (PPN or TPN). Postoperative management includes ventilatory weaning and extubation as soon as possible. An esophagram is obtained on approximately postoperative day 5 to evaluate for a leak. If there is no leak after surgical intervention, feeds can be started. Antireflux medication is usually recommended postoperatively (Slater & Rothenberg, 2016).
Gastroschisis and Omphalocele
Gastroschisis and omphalocele are the two most common congenital abdominal wall defects. Both have an incidence of around 1 in 4,000 live births, though omphalocele is found 1 in 1,100 during second trimester ultrasound scans. The frequency of fetal demise for omphalocele is almost 3 in 4. The incidence of gastroschisis has been increasing over the past few decades without any known cause, though socioeconomic status and environmental factors have been linked to the rise (Bence & Wenger, 2021).
Etiology
One common abdominal wall defect is gastroschisis , which is found to the right side of the umbilicus where the protective covering over the herniated abdominal contents is missing. The fetal development defect is not fully understood, but it may be from disruption of movement of the lateral ventral body folds early in embryonal development (Bence & Wenger, 2021).
The other common abdominal wall defect is omphalocele , which occurs at the abdominal midline and is thought to be due to a folding defect that happens as the bowel returns to the abdominal cavity during expected development. The defect involves the umbilical ring and is encased by a three-layer sac—peritoneum, Wharton’s jelly, and amnion (Figure 25.10).
Diagnostics
Over 90 percent of fetuses with gastroschisis are diagnosed in utero by ultrasound showing free-floating intestines. Most are found in the second trimester, as the full rotation and completion of gut development does not occur until the end of the first trimester (Bence & Wenger, 2021).
Omphalocele defects can range widely in size and severity and are more often found with concurrent congenital anomalies or comorbidities—chromosomal, cardiac, genitourinary, musculoskeletal, gastrointestinal, and/or neurologic (Bence & Wenger, 2021). Similarly, omphalocele defects are also found on ultrasound, though diagnosis occurs at the end of the first trimester, around half the time with the ultrasound finding herniated abdominal contents midline (Slater & Pimpalwar, 2020).
Nursing Management
Current practice is mixed for gastroschisis, with some providers initiating early delivery (prior to 37 weeks’ gestational age) and others waiting until the fetus is full term for delivery. Delivery vaginally or via cesarean section has not been found to have a significant effect on the newborn. Practice for omphalocele is less mixed. Because of the higher risk for sac rupture during vaginal delivery, term delivery via cesarean section is more common (Bence & Wenger, 2021). Preparing the birthing parent for frequent testing, nonstress test (NST), biophysical profile (BPP), and sonographic amniotic fluid index weekly to monitor for fetal distress or demise is a part of the nursing role, along with preparation for either an induced or a cesarean delivery.
In the past couple of decades, novel approaches to the treatment of gastroschisis before surgery as a newborn have been added to the potential treatment list. One is amnioexchange, where the amniotic fluid is removed and normal saline is used to replace it because amniotic fluid is inflammatory to the bowels that are exposed in utero. Another potential prenatal treatment could be a fetoscopic intervention, where the intestines are covered in utero or they are placed into the abdominal space and the defect is surgically closed (Bence & Wenger, 2021).
Small omphalocele defects are surgically closed in the newborn with one surgery. Staged surgeries may be required if the amount of the bowel content within the sac is large (Bence & Wenger, 2021). MRI while in utero may be helpful in determining the size of the defect and what to expect for the newborn surgically after birth.
The neonate with gastroschisis or omphalocele is cared for in a NICU both before and after surgery. Frequent monitoring of intake and output, temperature, and signs and symptoms of infection is required. Educating the family about prenatal treatment options and the likely need for surgery to close the defect after birth is the nursing role.
Clubfoot
One common congenital limb deformity is congenital talipes equinovarus (CTEV) , or clubfoot . It has a range of presentations with different degrees of involvement and severity (Canavese & Dimeglio, 2021).
Etiology
Approximately 1 to 3 in 1,000 live white infant births are affected with clubfoot. Prevalence is variable between ethnic groups, with people of Polynesian ancestry having the highest prevalence at 7 in 1,000 live births. Males are affected twice as often as females (Magriples, 2021). A genetic origin has been determined by clinical studies over the past century, but the gene responsible has not yet been identified (Ippolito & Gorgolini, 2021).
Pathophysiology
Clubfoot is an isolated idiopathic congenital disorder in which 80 percent of cases are not associated with any chromosomal or genetic anomalies or underlying disease process. Clubfoot is an intrinsic outcome of some neurologic, muscular, skeletal, or connective tissue diseases and is found to be included in over 50 identifiable syndromes, spina bifida being the most common (Magriples, 2021). External environmental factors affecting the fetus can also cause clubfoot. Instances of growth impedance in multiple gestation, malpresentation, uterine cavity abnormalities like fibroids or amniotic bands, breech position, or oligohydramnios can all cause clubfoot (Magriples, 2021).
Risk factors for clubfoot include family history of relatives with the congenital defect, extrinsic conditions that restrict fetal foot growth and movement, a fetal neuromuscular disorder, maternal or paternal tobacco use, maternal obesity, early amniocentesis (done before 15 weeks’ gestation), maternal use of selective serotonin reuptake inhibitors (SSRIs), and male sex (Chen et al., 2018).
Nursing Management
Nursing management for the newborn with clubfoot includes direct assessment of the lower limbs, their range of motion, and presentation. The nurse’s role is primarily to give information to the birth parent or family of the newborn, educating them on the future plan of care and the ultimate goals of mobility, and alleviating any underlying concerns or fears they may have about clubfoot.
The gold standard treatment for clubfoot is the Ponseti method , serial manipulation of the foot and ankle with casting and percutaneous Achilles tenotomy followed by long-term use of a foot abduction brace (Figure 25.11)
While the limb or limbs are cast, the nurse assesses for adequate perfusion distal to the cast and identifies any skin breakdown or area that is at risk for skin breakdown. As casting occurs, the calf muscles may become atrophied, or smaller than expected, resulting in pain or soreness with activity. Nonpharmacologic interventions such as heat or cold packs and massage can be provided and encouraged at home.
If treatment for clubfoot is not provided, lifelong disability, deformity, and pain result. Surgical treatment may be required. There are a variety of surgical procedures (Gelfer et al., 2022; Magriples, 2021).
Infants of Pregnant People with Diabetes
Neonates born to a person with diabetes—gestational, type 1, or type 2—are more likely to have adverse outcomes. High blood glucose at time of conception can even affect the outcome of the pregnancy, with a greater risk of stillbirth, preterm birth, and congenital birth defects (CDC, 2018). Congenital anomalies are 3 times more likely in infants of people with diabetes than in infants who do not experience the uterine environment of diabetes. Central nervous system defects such as anencephaly and spina bifida occur 16 times more often, and cardiac anomalies occur in 30 percent of infants born to people with diabetes (Carlo & Ambalavanan, 2016). In addition, newborns born to pregnant persons with diabetes are at risk for birth injury due to increased neonatal size (CDC, 2018).
Signs and Symptoms
The infant born to a person with diabetes will be at risk for hypoglycemia after birth. Classic presentations of an infant born to a diabetic birthing person include macrosomia , or a size larger than expected for gestational age in a neonate, and being heavily coated with vernix. The hypoglycemic infant can be asymptomatic, though tremors or jitteriness is the most common sign and symptom, if one is seen. The infant can also have a large placenta to go along with their large size. Infants born to people with advanced diabetes may be the opposite: small for gestational age or having intrauterine growth restriction (IUGR). All infants with a maternal history of DM will have an increased occurrence of hypocalcemia, hyperbilirubinemia, hypomagnesemia, and respiratory distress syndrome (Shah et al., 2022) in the neonatal period.
Nursing Management
Managing these infants requires close monitoring of serum glucose levels and frequent assessment to evaluate for respiratory distress and hypothermia . If the infant is stable, feeding by mouth within the first hour of life is the best nutritional plan (Shah et al., 2022). The newborn may respond robustly to dextrose-containing fluids because of their sensitivity to insulin release. Due to the increased size of some of these infants, delivery injuries can be common. Early identification leads to early treatment and best outcomes.
Drug-Exposed Infant
Infants born to persons who have used drugs during pregnancy will have a variety of symptoms related to the agent or agents they are withdrawing from. This substance use can result in neonatal abstinence syndrome (NAS) , which occurs when the newborn has been exposed to drugs, legal or illegal, that are no longer available, resulting in withdrawal. These signs can potentially include tremors, irritability, disorganized feeding, and an inability to be consoled. Newborns will usually begin exhibiting withdrawal symptoms within 24 to 36 hours after birth, but the onset of symptoms may be delayed up to 7 days. Newborns exposed to alcohol while in utero exhibit withdrawal symptoms at only 3 to 12 hours after birth (Schaff et al., 2019).
Signs and Symptoms
Newborns in withdrawal have been connected to their birthing parent’s bloodstream. Whatever substances the birthing parent ingests, the fetus is exposed to. When the fetus is delivered, their supply has been abruptly stopped. The most common symptoms seen in newborns withdrawing from any kind of addictive substances—opioids, narcotics, benzodiazepines, nicotine, or alcohol—are excessive high-pitched crying, hyperactive Moro reflexes, mild to moderate tremors in one or both hands or feet, increased muscle tone, myoclonic jerks (twitching/jerking) of their limbs or face, hyperthermia, frequent yawning, sneezing, and respiratory distress. Additionally, the nurse will notice that the infant has gastrointestinal symptoms. These include disorganized feeding that appears as excessive sucking, uncoordinated sucking leading to frustration, projectile vomiting, and loose and watery stool (Chin Foo et al., 2021). Table 25.5 lists the neurologic signs of drug withdrawal in the newborn.
| Maternal or Medical Substance | Neurologic Symptoms in Newborn |
|---|---|
| Nicotine | Increased Moro reflex, excessive high-pitched cry, tremors, sleep problems, hypertonia, seizures, fever, inconsolability |
| Alcohol | High-pitched cry, sleep problems, decreased suck reflex, poor coordination with feeding, hyperreflexia, inconsolability |
| Marijuana | Jitteriness and irritability (Hale & Phillips, 2022) |
| Opioids (maternal exposure or medical treatment) | Tremors, hyperreflexia, hypertonia, inconsolability, high-pitched cry, poor coordination with feeds, respiratory distress, sleep problems, diarrhea, sneezing, jaundice, seizures, death |
| Cocaine | Tremors, hyperreflexia, hypertonia, inconsolability, high-pitched cry, poor coordination with feeds, respiratory distress, sleep problems, diarrhea, sneezing, jaundice, seizures, death |
| Benzodiazepines | Tremors, hyperreflexia, hypertonia, inconsolability, high-pitched cry, poor coordination with feeds, respiratory distress, sleep problems, diarrhea, sneezing, jaundice, seizures, death |
Diagnostics
If the newborn is exhibiting any withdrawal symptoms, the nurse can use the Finnegan Neonatal Abstinence Scoring Tool (FNAST) (Bagley et al., 2014) to determine how to manage care. Serial scores are used to measure the infant’s progress.
The Finnegan Neonatal Abstinence Scoring Tool (FNAST) is one way to evaluate and monitor neonates who are experiencing substance withdrawal.
Management
Different facilities will have slightly different protocols for managing infants with NAS. The Finnegan Management Algorithm is one example. The use of FNAST scoring helps the nurse monitor the newborn’s need for more intense intervention, such as being transferred to the NICU. Specialists in the NICU can then manage the newborn’s medication to help with withdrawal symptoms and prevent the newborn from becoming overwhelmed. The treatment can include benzodiazepines, alpha adrenergics, or weaning off the opioid over time. Newborns who experience withdrawal symptoms are at risk for seizures, respiratory failure, and failure to thrive.
This site shows one example of a protocol for managing infants with NAS using the Finnegan Management Algorithm.


26.E: Nervous System Infections (Exercises)
26.1: Anatomy of the Nervous System
The human nervous system can be divided into two interacting subsystems: the peripheral nervous system (PNS) and the central nervous system (CNS). The CNS consists of the brain and spinal cord. The peripheral nervous system is an extensive network of nerves connecting the CNS to the muscles and sensory structures.
Multiple Choice
What is the outermost membrane surrounding the brain called?
- pia mater
- arachnoid mater
- dura mater
- alma mater
- Answer
-
C
What term refers to an inflammation of brain tissues?
- encephalitis
- meningitis
- sinusitis
- meningoencephalitis
- Answer
-
A
Nerve cells form long projections called ________.
- soma
- axons
- dendrites
- synapses
- Answer
-
B
Chemicals called ________ are stored in neurons and released when the cell is stimulated by a signal.
- toxins
- cytokines
- chemokines
- neurotransmitters
- Answer
-
D
The central nervous system is made up of
- sensory organs and muscles.
- the brain and muscles.
- the sensory organs and spinal cord.
- the brain and spinal column.
- Answer
-
D
Matching
Match each strategy for microbial invasion of the CNS with its description.
| ___intercellular entry | A. pathogen gains entry by infecting peripheral white blood cells |
| ___transcellular entry | B. pathogen bypasses the blood-brain barrier by travel along the olfactory or trigeminal cranial nerves |
| ___leukocyte-facilitated entry | C. pathogen passes through the cells of the blood-brain barrier |
| ___nonhematogenous entry | D. pathogen passes between the cells of the blood-brain barrier |
- Answer
-
D, C, A, B
Fill in the Blank
The cell body of a neuron is called the ________.
- Answer
-
soma
A signal is transmitted down the ________ of a nerve cell.
- Answer
-
axon
The ________ is filled with cerebrospinal fluid.
- Answer
-
subarachnoid space
The ________ ________ prevents access of microbes in the blood from gaining access to the central nervous system.
- Answer
-
blood-brain barrier
The ________ are a set of membranes that cover and protect the brain.
- Answer
-
meninges
Short Answer
Briefly describe the defenses of the brain against trauma and infection.
Describe how the blood-brain barrier is formed.
Identify the type of cell shown, as well as the following structures: axon, dendrite, myelin sheath, soma, and synapse.
Critical Thinking
What important function does the blood-brain barrier serve? How might this barrier be problematic at times?
26.2: Bacterial Diseases of the Nervous System
Bacterial infections that affect the nervous system are serious and can be life-threatening. Fortunately, there are only a few bacterial species commonly associated with neurological infections.
Multiple Choice
Which of the following organisms causes epidemic meningitis cases at college campuses?
- Haemophilus influenzae type b
- Neisseria meningitidis
- Streptococcus pneumoniae
- Listeria monocytogenes
- Answer
-
B
Which of the following is the most common cause of neonatal meningitis?
- Haemophilus influenzae b
- Streptococcus agalactiae
- Neisseria meningitidis
- Streptococcus pneumoniae
- Answer
-
B
What sign/symptom would NOT be associated with infant botulism?
- difficulty suckling
- limp body
- stiff neck
- weak cry
- Answer
-
C
Which of the following can NOT be prevented with a vaccine?
- tetanus
- pneumococcal meningitis
- meningococcal meningitis
- listeriosis
- Answer
-
D
How is leprosy primarily transmitted from person to person?
- contaminated toilet seats
- shaking hands
- blowing nose
- sexual intercourse
- Answer
-
C
Fill in the Blank
The form of meningitis that can cause epidemics is caused by the pathogen ________.
- Answer
-
Neisseria meningitidis
The symptoms of tetanus are caused by the neurotoxin ________.
- Answer
-
tetanospasmin
________ is another name for leprosy.
- Answer
-
Hansen’s disease
Botulism prevents the release of the neurotransmitter ________.
- Answer
-
acetylcholine
________ is a neurological disease that can be prevented with the DTaP vaccine.
- Answer
-
Tetanus
Tetanus patients exhibit ________ when muscle spasms causes them to arch their backs.
- Answer
-
opisthotonos
Short Answer
A physician suspects the lesion and pustule pictured here are indicative of tuberculoid leprosy. If the diagnosis is correct, what microorganism would be found in a skin biopsy?
(credit: Centers for Disease Control and Prevention)
Critical Thinking
Explain how tetanospasmin functions to cause disease.
The most common causes of bacterial meningitis can be the result of infection by three very different bacteria. Which bacteria are they and how are these microbes similar to each other?
Explain how infant botulism is different than foodborne botulism.
26.3: Acellular Pathogenic Diseases of the Nervous System
A number of different viruses and subviral particles can cause diseases that affect the nervous system. Viral diseases tend to be more common than bacterial infections of the nervous system today. Fortunately, viral infections are generally milder than their bacterial counterparts and often spontaneously resolve. Some of the more important acellular pathogens of the nervous system are described in this section.
Multiple Choice
Which of these diseases can be prevented with a vaccine for humans?
- eastern equine encephalitis
- western equine encephalitis
- West Nile encephalitis
- Japanese encephalitis
- Answer
-
D
Which of these diseases does NOT require the introduction of foreign nucleic acid?
- kuru
- polio
- rabies
- St. Louis encephalitis
- Answer
-
A
Which of these is true of the Sabin but NOT the Salk polio vaccine?
- requires four injections
- currently administered in the United States
- mimics the normal route of infection
- is an inactivated vaccine
- Answer
-
C
Which of the following animals is NOT a typical reservoir for the spread of rabies?
- dog
- bat
- skunk
- chicken
- Answer
-
D
Fill in the Blank
The rogue form of the prion protein is called ________.
- Answer
-
PrP Sc
________ are the most common reservoir for the rabies virus worldwide.
- Answer
-
Dogs
________ was the scientist who developed the inactivated polio vaccine.
- Answer
-
Jonas Salk
________ is a prion disease of deer and elk.
- Answer
-
Chronic wasting disease
The rogue form of prion protein exists primarily in the ________ conformation.
- Answer
-
beta sheet
Short Answer
Explain how a person could contract variant Creutzfeldt-Jakob disease by consuming products from a cow with bovine spongiform encephalopathy (mad cow disease).
Critical Thinking
If the Sabin vaccine is being used to eliminate polio worldwide, explain why a country with a near zero infection rate would opt to use the Salk vaccine but not the Sabin vaccine?
26.4: Neuromycoses and Parasitic Diseases of the Nervous System
Fungal infections of the nervous system, called neuromycoses, are rare in healthy individuals. However, neuromycoses can be devastating in immunocompromised or elderly patients. Several eukaryotic parasites are also capable of infecting the nervous system of human hosts. Although relatively uncommon, these infections can also be life-threatening in immunocompromised individuals. In this section, we first discuss neuromycoses, followed by parasitic infections of the nervous system.
Multiple Choice
Which of these diseases results in meningitis caused by an encapsulated yeast?
- cryptococcosis
- histoplasmosis
- candidiasis
- coccidiomycosis
- Answer
-
A
What kind of stain is most commonly used to visualize the capsule of cryptococcus?
- Gram stain
- simple stain
- negative stain
- fluorescent stain
- Answer
-
C
Which of the following is the causative agent of East African trypanosomiasis?
- Trypanosoma cruzi
- Trypanosoma vivax
- Trypanosoma brucei rhodanese
- Trypanosoma brucei gambiense
- Answer
-
C
Which of the following is the causative agent of primary amoebic meningoencephalitis?
- Naegleria fowleri
- Entameba histolyticum
- Amoeba proteus
- Acanthamoeba polyphaga
- Answer
-
A
What is the biological vector for African sleeping sickness?
- mosquito
- tsetse fly
- deer tick
- sand fly
- Answer
-
B
How do humans usually contract neurocysticercosis?
- the bite of an infected arthropod
- exposure to contaminated cat feces
- swimming in contaminated water
- ingestion of undercooked pork
- Answer
-
D
Which of these is the most important cause of adult onset epilepsy?
- neurocysticercosis
- neurotoxoplasmosis
- primary amoebic meningoencephalitis
- African trypanosomiasis
- Answer
-
A
Fill in the Blank
The ________ is the main virulence factor of Cryptococcus neoformans .
- Answer
-
capsule
The drug of choice for fungal infections of the nervous system is ________.
- Answer
-
Amphotericin B
The larval forms of a tapeworm are known as ________.
- Answer
-
cysticerci
________ sign appears as swollen lymph nodes at the back of the neck in early African trypanosomiasis.
- Answer
-
Winterbottom’s
________ African trypanosomiasis causes a chronic form of sleeping sickness.
- Answer
-
West
The definitive host for Toxoplasma gondii is ________.
- Answer
-
cats
Trypanosomes can evade the immune response through ________ variation.
- Answer
-
antigenic
Short Answer
Why do nervous system infections by fungi require such long treatment times?
Briefly describe how humans are infected by Naegleria fowleri .
Briefly describe how humans can develop neurocysticercosis.
Critical Thinking
The graph shown tracks the body temperature of a patient infected with Trypanosoma brucei . How would you describe this pattern, and why does it occur?
(credit: modification of work by Wellcome Images)
Fungal meningoencephalitis is often the ultimate cause of death for AIDS patients. What factors make these infections more problematic than those of bacterial origin?
Compare East African trypanosomiasis with West African trypanosomiasis.


12.4: Communication Competence
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In this section, we will address techniques you can use to communicate your opinions, rights, expectations and boundaries. We will also look at the relationship between culture, co-culture, and power, and at some ways in which power is often misused in intimate relationships.
Effective Communication: Communicating Opinions, Rights, Expectations, and Boundaries
Since power dynamics influence our interactions and relationships, we may find ourselves in positions where we have less power or perceive we have less power. In these situations, it is important to know how to effectively communicate our opinions, rights, expectations, and boundaries. Below we provide some strategies you can use:
Be assertive, not passive or aggressive.
Passive behaviors include concealing rather than communicating our feelings, thoughts, rights, and expectations. Often times, people engage in passive behaviors when they perceive they have little power, or they fear damaging a relationship. Aggressive behaviors include yelling, threatening, name calling, etc.
Assertive communication carries respect for the feelings, needs, wants, and opinions of others. An assertive communicator avoids infringing upon the rights of others, while asserting their own, and seeking compromise or collaboration in the process. Assertive communication utilizes actions and words to express opinions, rights, expectations, and boundaries in a calm fashion, while conveying a message of confidence and respect. [1] When communicating assertively, you should not make sarcastic or condescending remarks, blame the other, shout, threat, or name call.
Don’t be silent if you have something to say.
When you have an opinion or feel your rights or expectations are being violated in some way, voice it. Just make sure you pick the right moment and use assertive—not aggressive—communication. Also, make it clear that what you have to say is important, valid, and/or should be noticed.
Identify what your needs are.
Identify your own needs and what makes you happy. This will help you develop a set of expectations that you wish others would follow as to how you would like to be treated. To help with identifying your needs, situations- past or present-where you don’t feel like you’re being treated with mutual respect or situations where you sense your feelings weren’t considered. Then speculate about what might make you feel more respected.
[27]
Say “no” when appropriate.
It’s okay to reject someone, to say no, or to not do something that is desired of you. Saying no can be difficult for many people. However, saying “yes” when you need to say “no” can lead to unnecessary stress, resentment, and anger toward others. When saying no, it can be helpful to keep in mind a useful set of guidelines:
[13]
- Keep it brief.
- Be clear.
- Be honest.
For example, if you don’t have time to do a favor, you can simply say, “I can’t this time. Sorry to disappoint you, but I have too many things to do that day, and there’s no room in my schedule.” Also, if someone asks you a question that you don’t want to answer, it okay to say something like “I don’t really feel comfortable answering that.”
Have confident body language.

Contextual Communication: Culture, Co-Culture, and Power
Power is also influenced by culture and co-culture. As mentioned in Chapter 2: Culture and Communication, all cultures consist of a dominant group and nondominant group. Group memberships and identities, such as gender and race, can work to advantage one particular group of people while simultaneously disadvantaging another to create unequal power dynamics and oppression. Such actions are accomplished, as discussed below, through labeling, othering, and stereotyping. Also covered below is ways in which ideologies operate to mask these inequalities.
Labeling, Othering, and Stereotyping
The dominant group engages in exercises of power that reflect their interests and help to perpetuate inequalities in power and status. Systems of power and domination are maintained at a cultural and co-cultural level through labeling, othering, and stereotyping. The labels attached to people seen as ‘minorities’ have always been defined by the white majority—that is, by those with power. Defining an individual primarily in terms of their apparent racial or ethnic identity—for example, with labels such as black or Asian—is a way of defining them as ‘different’ from a supposed white ‘norm.’ Othering is accomplished by creating an insider/outsider narrative where whiteness is the criteria for normal; you are either white or non-white. The same can be said of attaching labels to people on the basis of a supposed disability, sexual preference, or age. In addition, stereotyping makes broad generalizations about groups and people based on their co-cultural membership and identities. Often, these stereotypes are negative, since they reflect the differential power between those in the ‘majority’ and those categorized as ‘minorities’ or ‘different.’ So, for example, women may be defined as less rational than men, or black people as less intelligent than white people; in these instances, men and white people respectively are characterized as the ‘norm.’ These negative stereotypes both reflect and perpetuate existing inequalities—patterns of sexism and racism in society. An example would be denying women and people of color access to jobs that require a ‘cool head’ or complex intellectual skills. In other words, stereotyping people as ‘different’ often leads to prejudice and discrimination. Attributing these fixed ‘differences’ to people is not a neutral process, but is one that both reflects and reproduces inequalities of power and status.
Ideologies
Another way we see power maintained and normalized at a cultural level is through the use of ideologies and values. In the United States, there are many overlapping ideologies that create the illusion that inequality linked to co-cultural categories, such as race or social class, do not exist. For example, a prevalent U.S. American ideology is the Achievement Ideology which is the belief that any person can be successful through hard work and education and that disadvantaged individuals need to “pull themselves up by their bootstraps.” This ideology disadvantages particular groups by placing the blame of success or failure on the individual rather than looking at institutional and systemic inequality—or, “lack of bootstraps.” For example, K-12 educational institutions have become increasingly segregated by race and social class, and, as such, students who attend certain schools don’t have access to the same quality of educational resources as another group may have. Unequal access impacts academic performance and makes some students more likely to attain high grades or perform well on the college admissions tests necessary to get into universities (Orfield and Frankenberg’s, 2014). In addition, inside the classroom, it is the dominant group’s behaviors and values that have been normalized. These norms determine what a successful student looks and acts like, as well as how they are evaluated in assessments like tests and papers (Bennett & Lecompte, 1990; Lesdesma & Caldera, 2005). Students who violate teacher expectations for “normal” behavior face consequences and are “judged by teachers to be less academically able (Bennett & LeCompte, 1990, p. 16).” Such treatment disadvantages low income and students of color who may have different, conflicting, or even contradictory cultural norms and values. People of color and ESL students are also more likely than their white counterparts to be tracked into remedial courses and thus they do not receive the same quality of education. These types of systemic inequalities in K-12 education hold long-term implications for the success of these groups
Reflective Communication: Misuses of Power in Intimate Relationships
Generally, healthy relationships contain a relative balance of power between participants. Unhealthy relationships occur when there are imbalances of power and one participant tries to control or take advantage of the other. This is accomplished by using abusive power to gain and maintain control and subject that person to psychological, physical, sexual, or financial abuse. The goal of the abuser is to control and intimidate the victim or to influence them to feel that they do not have an equal voice in the relationship[2] and abusers usually to try normalize, legitimize, rationalize, deny, minimize the abusive behavior, or blame the victim for it.[7][8][9] Controlling abusers use multiple tactics to exert power and control over their partners. Because each of the tactics are used to maintain power in the relationship, it is important to become familiar with the tactics below in order to avoid being part of an unhealthy relationship, or to help and educate others.
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Coercion and Threats:
Threats and coercion are tools for exerting control and power. Abusers may threaten to leave, hurt others, or even threaten suicide. They may also coerce others to perform illegal actions or to drop charges against their abusers. [36] At its most powerful, the abuser creates intimidation and fear through unpredictable and inconsistent behavior.[6]
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Intimidation:
Abused individuals may be intimidated by the brandishing of weapons—for example, threatening to use a gun or simply displaying the weapon. Other forms of intimidation include destruction of property or other things, or use of gestures or looks to create fear.[36]
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Economic Abuse:
Controlling someone’s access to money is another means of ensuring control and power over another. One method is to prevent the other from getting or retaining a job. Other ways to control access to money are: withholding information and access to family income, taking a person’s money, requiring the person to ask for money, giving someone an allowance, or filing a power of attorney or conservatorship—particularly in the case of economic abuse of the elderly.[36]
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Emotional Abuse:
Emotional abuse includes name-calling, mind games, putting the victim down, or humiliating the individual. The goals are to make the person feel bad about themselves, feel guilty or think that they are crazy.[36]
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Isolation:
Another element of psychological control is the isolation of the victim from the outside world.[33] Isolation includes controlling a person’s social activity—who they see, who they talk to, where they go, and any other method that limits access to others. It may include limiting what material is read, insisting on knowing where the victim is at all times, and requiring permission for medical care. The abuser might also exhibit hypersensitive and reactive jealousy.[33]
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Minimizing, Denying, and Blaming:
An abuser may deny that any abuse occurred in order to place the responsibility for their behavior on the victim. Another example of this type of control is when the abuser minimizes the victim’s concerns or denies the degree of abuse. [36]
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Using Children and Pets:
Children may be also be used to exert control. Abusers threaten to take the children or make the other feel guilty about the children. Abusers may harass children during visitation or use the children to relay messages. Abusing pets is another controlling tactic. [36]
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Using Privilege:
Using “privilege” means that the abuser defines the roles in the relationship, makes the important decisions, treats the individual like a servant, and acts like the “master of the castle”.[36]


10.1: Cladistics
The more contemporary, much more formalized than expert-based is cladistics . Below, cladistic procedure is explained using artificial example of three organisms. The goal of the analysis is the creation of a phylogeny tree ( cladogram ) which becomes the basis of classification. Below is a short instruction which explains the basics of the cladistic analysis on the artificial example of several “families” of plants.
1. Start with determining the “players”—all subtaxa from bigger group. In our case, it will be these three “families”:
Alphaceae
Betaceae
Gammaceae
2. Describe these three groups:
Alphaceae : Flowers red, petioles short, leaves whole, spines absent
Betaceae : Flowers red, petioles long, leaves whole, spines absent
Gammaceae : Flowers green, petioles short, leaves dissected, spines present
3. Determine individual characters (we will need at least \(2N+1\) characters where \(N\) is number of studied taxa):
(1) Flower color
(2) Petiole size
(3) Dissection of leaves
(4) Presence of spines
4. Polarize the characters : every character should have at least two character states where “0” is ancestral, plesiomorphic state, and “1” is derived, apomorphic state. To decide which state is plesiomorphic and which is apomorphic, use these kinds of arguments:
(a) Historical evidence (e.g., from fossils)
(b) Developmental evidence
(c) Comparative evidence
5. If this information is absent, find the outgroup which is the most ancestral, most early divergent taxon related to our groups. In our case, we will employ outgroup:
Omegaceae : Flowers green, petioles short, leaves whole, spines absent.
6. Label characters with “1” (apomorphic) or “0” (plesiomorphic):
(1) Flower color green—0; red—1
(2) Petiole size small—0; big—1
(3) Dissection of leaves absent—0; present—1
(4) Absence of spines—0; spines present—1
7. Make character table containing both subtaxa and labeled characters:
|
(1) |
(2) |
(3) |
(4) |
|
|---|---|---|---|---|
|
Alphaceae |
1 |
0 |
0 |
0 |
|
Betaceae |
1 |
1 |
0 |
0 |
|
Gammaceae |
0 |
0 |
1 |
1 |
(Outgroup, Omegaceae evidently has all zeroes.)
8. Start the tree from outgroup (this step is not absolutely necessary but will make phylogeny more clear):
9. Most ancient ingroup (Alphaceae) is a first branch, label it with bar which shows acquisition of the advanced state of first character (red flower color):
10. Attach more and more sub-taxa. It is possible to do this randomly (like most of phylogeny software), or attach groups to make shortest tree. For example, Betaceae and Gammaceae have equal number of synapomorphies but Betaceae have only one character different from Alphaceae it is sensible to attach it first, and then attach Gammaceae:
This tree has 4 evolutionary events (length \(=4\))
11. If Gammaceae was attached first, then resulted tree will be be one step longer:
There are five evolutionary events; in other words, length of tree \(=5\). (“p” are parallel characters (homoplasies); there might be also reversals (“r”), when apomorphic character disappears).
There could be also tree with length \(=6\), or even more if tree includes character reversals, but all of them will be longer than the first one.
12. Choose the shortest, most parsimonous tree. Second tree has 5 events, first tree has 4 events, others could be only longer. Consequently, we choose the first tree. By the way, many computer programs do not follow the procedure above strictly and simply produce all possible trees, and finally choose the shortest.
13. Use the chosen tree as a source of classification:
Order Alphales
1. Family Alphaceae
2. Family Betaceae
Order Gammales
1. Family Gammaceae
This step is needed only if you wish to convert cladogram into traditional, classification. In fact, cladograms are rank-free and might be used as is.
Cladograms often used as source of time trees which are made with genetic information and information from fossils. If we know the age of taxonomic group, we can use it as more objective replacement of rank.
Ability to review and compare phylogenetic trees requires understanding of several basic rules, for example:
1. Tree edges may be freely rotated in any direction. For example, these trees are same:
2. Direction of branches also does not matter. These trees are same:
It is not always simple to make classification from a tree. On the previous example, we simply designate the whole branch as a taxon (order which contains our three families). There are situations when only middle part of the branch seems to be acceptable as a taxon. In these cases, remaining part is called paraphyletic taxon.
Paraphyletic groups include all immediate ancestors of its members but not all descendants of these ancestors. Good example of paraphyletic taxon are reptiles: when we take mammals and birds from amniote branch, reptiles will be what is left. Gymnosperms (all seed plants without angiosperms) is another example, but in this case some molecular trees show that gymnosperms is also a natural branch (i.e., monophyletic group). Monophyletic groups include all immediate ancestors and all their descendants.
When the group contains taxa from different branches, it is polyphyletic . Polyphyletic groups are not allowed.
Another important distinction between groups of the phylogeny tree is stem and crown groups. All extant members together with their immediate ancestors form a crown of taxon (Figure \(\PageIndex{2}\)). If one member of crown went extinct, we can estimate that it was somehow similar to other crown members. In other words, if we find a way ho to re-create mammoth, we probably understand how to feed it because it belongs to the Elephantidae family crown. However, if the fossil, extinct members of taxon branch outside of crown ( stem groups), there are much less taxonomic estimations. It is hard to guess, for example, how to care for Archaeopteryx “dinosaur bird” because such organisms are not exist now and have no living similarities.


13.1: The Basics of Probability Theory
The probability of a specified event is the chance or likelihood that it will occur. There are several ways of viewing probability. One would be experimental in nature, where we repeatedly conduct an experiment. Suppose we flipped a coin over and over and over again and it came up heads about half of the time; we would expect that in the future whenever we flipped the coin it would turn up heads about half of the time. When a weather reporter says “there is a 10% chance of rain tomorrow,” she is basing that on prior evidence; that out of all days with similar weather patterns, it has rained on 1 out of 10 of those days.
Another view would be subjective in nature, in other words an educated guess. If someone asked you the probability that the Seattle Mariners would win their next baseball game, it would be impossible to conduct an experiment where the same two teams played each other repeatedly, each time with the same starting lineup and starting pitchers, each starting at the same time of day on the same field under the precisely the same conditions. Since there are so many variables to take into account, someone familiar with baseball and with the two teams involved might make an educated guess that there is a 75% chance they will win the game; that is, if the same two teams were to play each other repeatedly under identical conditions, the Mariners would win about three out of every four games. But this is just a guess, with no way to verify its accuracy, and depending upon how educated the educated guesser is, a subjective probability may not be worth very much.
We will return to the experimental and subjective probabilities from time to time, but in this course we will mostly be concerned with theoretical probability, which is defined as follows: Suppose there is a situation with \(n\) equally likely possible outcomes and that m of those \(n\) outcomes correspond to a particular event; then the probability of that event is defined as \(\frac{m}{n}\).
If you roll a die, pick a card from deck of playing cards, or randomly select a person and observe their hair color, we are executing an experiment or procedure. In probability, we look at the likelihood of different outcomes. We begin with some terminology.
The result of an experiment is called an outcome .
An event is any particular outcome or group of outcomes.
The sample space is the set of all possible simple events.
If we roll a standard 6-sided die, describe the sample space and some simple events.
The sample space is the set of all possible simple events: \(\{1,2,3,4,5,6\}\)
Some examples of events:
We roll a 1: outcome \(\{1\}\)
We roll a 5: outcome \(\{5\}\)
We roll a number bigger than 4: outcomes \(\{5,6\}\)
We roll an even number: outcomes \(\{2,4,6\}\)
Two dice are rolled. Write the sample space.
Solution
We assume one of the dice is red, and the other green. We have the following 36 possibilities.
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Green |
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Red |
1 |
2 |
3 |
4 |
5 |
6 |
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1 |
(1, 1) |
(1, 2) |
(1, 3) |
(1, 4) |
(1, 5) |
(1, 6) |
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2 |
(2, 1) |
(2, 2) |
(2, 3) |
(2, 4) |
(2, 5) |
(2, 6) |
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3 |
(3, 1) |
(3, 2) |
(3, 3) |
(3, 4) |
(3, 5) |
(3, 6) |
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4 |
(4, 1) |
(4, 2) |
(4, 3) |
(4, 4) |
(4, 5) |
(4, 6) |
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5 |
(5, 1) |
(5, 2) |
(5, 3) |
(5, 4) |
(5, 5) |
(5, 6) |
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6 |
(6, 1) |
(6, 2) |
(6, 3) |
(6, 4) |
(6, 5) |
(6, 6) |
The entry (2, 5), for example, indicates that the red die shows a 2 and the green shows a 5. This is different than the entry (5, 2) which indicates that the red die shows a 5 and the green die shows a 2.
A family has three children. Write a sample space.
Solution
The sample space consists of eight possibilities.
{ BBB, BBG, BGB, BGG, GBB, GBG, GGB, GGG }
The possibility BGB, for example, indicates that the first born is a boy, the second born a girl, and the third a boy.
We illustrate these possibilities with a tree diagram.
Given that all outcomes are equally likely, we can compute the probability of an event \(E\) using this formula:
\(P(E)=\frac{\text { Number of outcomes corresponding to the event } \mathrm{E}}{\text { Total number of equally likely outcomes }}\)
If we roll a 6-sided die, calculate
- P(rolling a 1)
- P(rolling a number bigger than 4)
Solution
Recall that the sample space is \(\{1,2,3,4,5,6\}\)
- There is one outcome corresponding to “rolling a 1”, so the probability is \(\frac{1}{6}\)
- There are two outcomes bigger than a 4, so the probability is \(\frac{2}{6}=\frac{1}{3}\)
Probabilities are essentially fractions, and should be reduced to lowest terms.
Let's say you have a bag with 20 cherries, 14 sweet and 6 sour. If you pick a cherry at random, what is the probability that it will be sweet?
Solution
There are 20 possible cherries that could be picked, so the number of possible outcomes is 20. Of these 20 possible outcomes, 14 are favorable (sweet), so the probability that the cherry will be sweet is \(\frac{14}{20}=\frac{7}{10}\).
There is one potential complication to this example, however. It must be assumed that the probability of picking any of the cherries is the same as the probability of picking any other. This wouldn't be true if (let us imagine) the sweet cherries are smaller than the sour ones. (The sour cherries would come to hand more readily when you sampled from the bag.) Let us keep in mind, therefore, that when we assess probabilities in terms of the ratio of favorable to all potential cases, we rely heavily on the assumption of equal probability for all outcomes.

- What is probability the minutes reading is 15?
- What is the probability the minutes reading is 15 or less?
- Answer
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There are 60 possible readings, from 00 to 59.
- \(\frac{1}{60}\)
- \(\frac{16}{60}\) (counting 00 through 15)
A standard deck of 52 playing cards consists of four suits (hearts, spades, diamonds and clubs). Spades and clubs are black while hearts and diamonds are red. Each suit contains 13 cards, each of a different rank : an Ace (which in many games functions as both a low card and a high card), cards numbered 2 through 10, a Jack, a Queen and a King.
Compute the probability of randomly drawing one card from a deck and getting an Ace.
Solution
There are 52 cards in the deck and 4 Aces so
\[P(A c e)=\dfrac{4}{52}=\frac{1}{13} \approx 0.0769 \nonumber\]
We can also think of probabilities as percents: There is a 7.69% chance that a randomly selected card will be an Ace.
Notice that the smallest possible probability is 0 – if there are no outcomes that correspond with the event. The largest possible probability is 1 – if all possible outcomes correspond with the event.
An impossible event has a probability of 0.
A certain event has a probability of 1.
The probability of any event must be \(0 \leq P(E) \leq 1\).
In the course of this chapter, if you compute a probability and get an answer that is negative or greater than 1, you have made a mistake and should check your work .


2.1.2: Scientific Method
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Science is a way to gain knowledge about natural phenomena using empirical observation and testing (Jurmain, et al 2013). While there are different protocols used in science, it is performed using a set of rules called The Scientific Method that guide scientific practice (Fancher 2000). The method stresses the need to develop a testable hypothesis, the use of objectivity and rationality, and the circularity of scientific research. This does not mean that science is infallible, but in using the scientific method, particularly with the necessity to have testable hypotheses and tests that are replicable by other researchers, rigorous conclusions are reached.
Why do students of biological anthropology need to understand the scientifc method? Because anthropology is a science.
Steps of the Scientific Method
Figure \(\PageIndex{1}\) - Diagram of the scientific method
1. Define the problem
This is based on observation -- either something you've observed from nature or from something that's already been written. How many times have you seen something or read about something and thought up a question about it? If you have, then you've done the first step of the Scientific Method!
2. Develop Hypothesis
Propose an explanation for the observed phenomenon. For a hypothesis to be a GOOD hypothesis, it must be testable. In other words, you must be ABLE to test it to see if it's supported or not supported. A hypothesis is still good, even if it's unsupported, as long as it's testable. There are lots of questions out there that are untestable, such as, "Somewhere on the planet, a pink elephant is dancing the can-can in a tutu." Because it's impossible to explore every inch of the world looking for our dancing elephant, this would not be feasibly testable. Along the same lines, a testable hypothesis would be, "Student group A, who have read the material on The Scientific Method, will have a higher average score on their quiz than will Student group B, who have not read the material on The Scientific Method."
3. Collect Data
The experiment should be specifically designed to test the hypothesis. The experiment will provide data as to whether the hypothesis is supported or not. Experiments must be replicable by other researchers. For our example above with ever-so-fortunate quiz-takers, you'd have Group A read the material (Group B would not) and both groups would take the quiz. This experimental design is replicable by other researchers because they too could find two groups of students, and follow the same protocol (one group reads the material, one not, and both take the quiz).
4. Organize/analyze data:
Once the experiment is completed, you must organize the data and analyze the results. For our example, you would grade the quizzes and calculate the average score per group.
5. Conclusion
You develop a statement that sums up what the data (collected during the experimental phase) says about the hypothesis. For our example, our concluding statement would be something like, "Group A, who read material on The Scientific Method, performed better on a Scientific Method quiz than did Group B, who did not read the material." If your hypothesis is supported, then you would move on to the next step in the process. If your hypothesis was not supported you would rework your hypothesis and start the process over.
6. Share the knowledge
It is important to share the results of your work even (and maybe even especially ) if your hypothesis was not supported. This hasn't been a step in the "old school version" of The Scientific Method, but remember -- information is only good if it's communicated to others!
Things to keep in mind:
- Science does not "prove" anything. Hypotheses are falsified/supported or not falsified/supported. For a hypothesis to be accepted as a theory, which is a generally accepted explanation of specific phenomena, it undergoes rigorous testing (Larsen 2008: 16). It can take decades for a hypothesis to become a theory.
- While we discuss various topics in biological anthropology that each piece of information was once a hypothesis that was tested and supported by the data. Contradictory supported-hypotheses are possible; some refer to this as equifinality . This just means that the data collected supports two (or more) hypotheses -- in most cases, there is not sufficient data available to support one more than the other (especially when we get to the information within human evolution). Hopefully, in these cases, one day we'll have enough evidence to overwhelmingly support one particular hypothesis, but at the present that's not possible. So, for the moment we have to open our minds to accept two potential conclusions.
The Scientific Method in Action!!! Watch the following clip and identify the steps of The Scientific Method. Was their hypothesis testable? Was their experiment replicable? What was the conclusion of their "scientific endeavor"? Clip: The Scientific Method in Action
References
- Fancher LJ. 2000. The Great “SM.” < www.cod.edu/people/faculty/fancher/scimeth.htm>. Accessed May 7, 2015.
- Jurmain R, Kilgore L, Trevathan W. Essentials of physical anthropology, 4th edition. Belmont (CA): Wadsworth, Cengage Learning; 2013. 437 p.
- Kaziek CJ, Pearson D. 2014. Ask a biologist: using the scientific method to solve mysteries. < http://askabiologist.asu.edu/explore/scientific-method >. Accessed May 7, 2015.
- Larsen CS. Our origins: discovering physical anthropology. New York (NY): W.W Norton & Company, Inc.; 2008. 430 p.


12.9: Gramática. El superlativo y el superlativo absoluto
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- Romano Sánchez Domínguez
- Imperial Valley College
Superlatives and absolute superlatives
Superlatives
Superlatives compare one versus all or the most and the least. Use the following constructions with superlatives:
Article + más + adjective + de + group being compared to. (Article and adjective must agree with gender and number of the subject of the sentence.)
Article + menos + adjective + de + group being compared to. (Article and adjective must agree with gender and number of the subject of the sentence.)
- El más inteligente de la clase. (The most intelligent in the class. This example refers to a male student because it uses the article "el".)
- María es la más bonita de su familia. (María is the most beautiful in her family. Use "la" since María is a female.)
- Juan y José son los más cómicos de su familia. (Juan and José are the most funny in their family. Use "los" to refer to Juan and José.)
- María y Mariela son las más bonitas de su clase. (María and Mariela are the most beautiful in their class. Use "las" to refer to María and Mariela.)
The absolute superlative
Absolute Superlative (in Spanish, "superlativo absoluto") is used with adjectives to express someone or something is extremely [+ adjective].
How to form absolute superlative
- Drop the last vowel of the adjective and add the ending “-ísimo", "-ísima", "-ísimos", "-ísimas" (depending on the gender and number of the noun it describes).
- If the adjective ends in the consonant “L”, just add “-ísimo”, "-ísima", "-ísimos", "-ísimas" to the adjective.
- If the adjective ends in the consonants “n” or “r”, add “-císimo", “-císima", “-císimos", “-císimas" to the adjective.
- If the original adjective has an accent mark, it must be transferred to the first "-í-" of "-ísimo".
Ejemplos
Note that all superlative endings and spell changes are indicated in bold .
| English | Spanish |
|---|---|
|
large My cell phone is extremely large. My purse is extremely large. |
grande Mi celular es grand ísimo . Mi bolsa es grand ísima . |
|
intelligent We are extremely intelligent. nice My friends are extremely nice. long My dress is extremely long. |
inteligente Somos inteligent ísimos . simpático ("c" changes to "qu") (same for rico, rica, poco, poca) Mis amigas son simpati qu ísimas . largo ("g" changes to "gu") Mi vestido es lar gu ísimo . |
|
difficult These classes are extremely difficult. |
difícil Estas clases son dificil ísimas . |
|
hard-working
young Your parents are extremely young. |
trabajador Mis padres son trabajador císimos . joven Tus padres son joven císimos . |


12.20: Defining Value
Learning Objectives
- Define value
“Value” is an overused and under-understood term in business today. Since we are wearing a retailer hat, we want to focus on value as it relates to our customers. For customers then, value is the perceived monetary worth of the combination of product, service, and utility provided.
The term “value proposition” is also a heavily-trafficked term used by business people today. Think of a value-proposition as an innovative feature intended to make a company or product attractive to customers. It can be best illustrated by a thought-scenario: You are shopping for media services to help you get the word out online about your new candy store. The first company comes to you with the following statement: “Trust me, our firm is number one and will give you the most for your money.” The second company comes to you with: “We can guarantee 200 clicks per day for every month of our contract.” Which value proposition would make you the most impressed?
For retailers, value can take on even more meaning. For example, there is a class of retail companies referred to as “value-price” retailers (generally discounted and/or inexpensive products). The largest home-shopping network uses value as part of their daily programming with a hook called “Today’s Special Value.” And when was the last time you were in a retail store and did not see some signage referring to “great value,” “best value,” or “value guarantee”? It is no wonder that our definition of “value” has become so murky.
Practice Questions
Contributors and Attributions
- Defining Value. Authored by : Bob Danielson. Provided by : Lumen Learning. License : CC BY: Attribution


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38: The Musculoskeletal System
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38.1: Types of Skeletal Systems - Functions of the Musculoskeletal System
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38.2: Types of Skeletal Systems - Types of Skeletal Systems
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38.3: Types of Skeletal Systems - Human Axial Skeleton
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38.4: Types of Skeletal Systems - Human Appendicular Skeleton
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38.5: Bone - Introduction
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Bones are made of a combination of compact bone tissue for strength and spongy bone tissue for compression in response to stresses.
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38.6: Bone - Cell Types in Bones
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The osteoblast, osteoclast, osteocyte, and osteoprogenitor bone cells are responsible for the growing, shaping, and maintenance of bones.
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38.7: Bone - Bone Development
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Intramembranous ossification stems from fibrous membranes in flat bones, while endochondral ossification stems from long bone cartilage.
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38.8: Bone - Growth of Bone
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38.9: Bone - Bone Remodeling and Repair
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38.10: Joints and Skeletal Movement - Classification of Joints on the Basis of Structure and Function
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38.11: Joints and Skeletal Movement - Movement at Synovial Joints
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38.12: Joints and Skeletal Movement - Types of Synovial Joints
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Synovial joints include planar, hinge, pivot, condyloid, saddle, and ball-and-socket joints, which allow varying types of movement.
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38.13: Joints and Skeletal Movement - Bone and Joint Disorders
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38.14: Muscle Contraction and Locomotion - Structure and Function of the Muscular System
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38.15: Muscle Contraction and Locomotion - Skeletal Muscle Fibers
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38.16: Muscle Contraction and Locomotion - Sliding Filament Model of Contraction
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38.17: Muscle Contraction and Locomotion - ATP and Muscle Contraction
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38.18: Muscle Contraction and Locomotion - Regulatory Proteins
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38.19: Muscle Contraction and Locomotion - Excitation–Contraction Coupling
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38.20: Muscle Contraction and Locomotion - Control of Muscle Tension
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