Family Health Exam 2-1B

Front 1

The nurse should tell a primigravida that the definitive sign indicating labor has begun would be

Back 1

Regular, progressive uterine contractions that increase in intensity and frequency are the definitive sign of true labor. Responses b and d are premonitory signs indicating the onset of labor is getting closer. Rupture of membranes usually occurs during labor itself.

Front 2

Which of the following laboratory test results would be a cause for concern if exhibited by an Rh-positive newborn 12 hours after birth?

Back 2

A reactive RPR/VDRL indicates exposure to syphilis while in utero. The negative Coombs indicates absence of antibodies against Rh-positive blood. Hgb is between 15 and 20 g/dl, and Hct is between 43 and 61%. The blood glucose level should be 45 mg/dl or higher.

Front 3

What is RDS caused by? What can result from it?

Back 3

RDS is caused by a lack of pulmonary surfactant, which leads to progressive atelectasis, loss of functional residual capacity, and ventilation-perfusion imbalance with an uneven distribution of ventilation.

Front 4

What can can increased pulmonary vascular resistance (PVR) from RDS lead to?

Back 4

Increased PVR can lead to right-to-left shunting and a reopening of the ductus arteriosus and foramen ovale.

Front 5

Clinical symptoms of RDS

Back 5

include tachypnea; grunting; nasal flaring; intercostal, or subcostal retractions; hypercapnia; respiratory or mixed acidosis; hypotension; and shock. These respiratory symptoms usually present immediately after birth or within 6 hours of birth.

Front 6

The treatment for RDS

Back 6

Adequate ventilation and oxygenation must be established and maintained in an attempt to prevent ventilation-perfusion mismatch and atelectasis. Exogenous surfactant, which alters the typical course of RDS, may be administered at or shortly after birth. Positive-pressure ventilation, CPAP, and oxygen therapy may be needed during the respiratory illness. Prevention of complications associated with mechanical ventilation is critical.

Front 7

What is the most common type of brain injury that occurs in neonates?

Back 7

Periventricular-intraventricular hemorrhage (PV-IVH)

Front 8

The pathogenesis of PV-IVH

Back 8

includes intravascular factors (e.g., fluctuating or increasing cerebral blood flow, increases in cerebral venous pressure, and coagulopathy), vascular factors, extravascular factors (hypoglycemia, acidosis), and routine nursery care (rapid volume expansion, blood transfusion). PV-IVH events typically occur within the first week of life.

Front 9

What is Necrotizing enterocolitis (NEC)?

Back 9

An acute inflammatory disease of the GI mucosa, commonly complicated by perforation.

Front 10

What is Surfactant?

Back 10

A surface-active phospholipid secreted by the alveolar epithelium. Acting much like a detergent, this substance reduces the surface tension of fluids that line the alveoli and respiratory passages, resulting in uniform expansion and maintenance of lung expansion at low intraalveolar pressure.

Front 11

How can surfactant be administered?

Back 11

Surfactant can be administered as an adjunct to oxygen and ventilation therapy. Generally, infants born before 32 weeks of gestation do not have adequate amounts of pulmonary surfactant to survive extrauterine life. In many centers the use of prophylactic surfactant is reserved for infants younger than 29 weeks who will likely have RDS (Hagedorn et al, 2002). Exogenous surfactant is manufactured artificially or extracted from bovine, porcine, or calf lung extract and is given as one or more doses through an endotracheal tube. The infant must be monitored for the occurrence of potential side effects such as patent ductus arteriosus and pulmonary hemorrhage. Although use of this medication has been associated with a significantly reduced length of time on mechanical ventilation and oxygen therapy and an increased survival rate in premature infants, it has not significantly decreased the incidence of CLD, intraventricular hemorrhage, or patent ductus arteriosus.

Front 12

PPHN

Back 12

A term applied to the combined findings of pulmonary hypertension, right-to-left shunting, and a structurally normal heart.

Front 13

What is PPHN also called?

Back 13

Also called persistent fetal circulation (PFC) because the syndrome includes reversion to fetal pathways for blood flow.

Front 14

What are some symptoms of PPHN?

Back 14

The infant with PPHN is typically born at term or postterm and presents with tachycardia and cyanosis and within minutes or hours progresses to severe respiratory compromise with concomitant acidosis, which further compromises pulmonary perfusion and deteriorating oxygenation.

Front 15

Signs of hypoglycemia

Back 15

jitteriness, twitching, lethargy, apathy, seizures, cyanosis, sweating, eye rolling, and refusal to eat. Cold stress, hypoxia, and respiratory distress can predispose infant to hypoglycemia.

Front 16

What is the most often fractured bone during birth?

Back 16

Clavicle

Front 17

clinical manifestations of Erb palsy

Back 17

the muscles of the hand are paralyzed, with consequent wrist drop and relaxed fingers. In a third and more severe form of brachial palsy, the entire arm is paralyzed and hangs limp and motionless at the side. The Moro reflex is absent on the affected side for all of the forms of brachial palsy. Total plexus is the second most common type of plexus injury

Front 18

Nursing care of the newborn with brachial palsy

Back 18

Concerned primarily with proper positioning of the affected arm. The affected arm should be gently immobilized on the upper abdomen. Passive range-of-motion exercises of the shoulder, wrist, elbow, and fingers are initiated in the latter part of the first week

Front 19

What is the most common type of ICH occuring in term infants ?

Back 19

Subarachnoid hemorrhage

Front 20

Subarachnoid hemorrhage

Back 20

A result of trauma and in preterm infants as a result of hypoxia. Small hemorrhages are the most common. Bleeding is of venous origin, and underlying contusion also may occur.

Front 21

The clinical presentation of subarachnoid hemorrhage

Back 21

In many infants, signs are absent, and hemorrhaging is diagnosed only because of abnormal findings on lumbar puncture, for example, red blood cells (RBCs) in the cerebrospinal fluid (CSF) or a hemorrhage is seen on a computerized tomography (CT) scan. The initial clinical manifestations of neonatal subarachnoid hemorrhage may be the early onset of alternating central nervous system (CNS) depression and irritability, with refractory seizure. Poor feeding, apnea, and unequal pupils may suggest an intracranial insult. Occasionally the infant appears normal initially then has seizures on the second or third day of life, followed by no apparent sequelae.

Front 22

nursing care of an infant with ICH

Back 22

It's supportive and includes monitoring neurologic signs and intravenous therapy, observation and management of seizures, and prevention of increased ICP.

Front 23

subdural hematoma

Back 23

A life-threatening collection of blood in the subdural space, most often is produced by the stretching and tearing of the large veins in the tentorium of the cerebellum, the dural membrane that separates the cerebrum from the cerebellum. When this type of bleeding occurs, the typical history includes a primiparous mother, with the total labor and birth occurring in less than 2 or 3 hours; a difficult birth involving high or midforceps application; or a large-for-gestational-age infant. Subdural hematoma occurs infrequently because of improvements in obstetric care.

Front 24

Why is a subdural hematoma so serious?

Back 24

it is especially serious because of its inaccessibility to aspiration by subdural tap.

Front 25

What are some inborn errors of metabolism?

Back 25

phenylketonuria (PKU), galactosemia, hemoglobinopathy (sickle cell disease and thalassemias) and hypothyroidism

Front 26

What causes IEMs?

Back 26

An inborn error of metabolism (IEM) is the term applied to a large group of disorders caused by a metabolic defect that results from the absence of or change in a protein, usually an enzyme, and mediated by the action of a certain gene. These defects can involve any substrate produced from protein, carbohydrate, or fat metabolism. Inborn errors of metabolism are recessive disorders, and a person must receive a defective gene from each parent for them to occur.

Front 27

Phenylketonuria (PKU)

Back 27

PKU results from a deficiency of the enzyme phenylalanine dehydrogenase. The test for PKU is not reliable until the newborn has ingested an ample amount of the amino acid phenylalanine, a constituent of both human and cow's milk. The nurse must document the initial ingestion of milk and perform the test at least 24 hours after that time. The current trend toward early infant discharge from the hospital has the potential to cause neonates with a disorder such as PKU not to be screened as often as in the past.

Front 28

What is the nursing care for PKU?

Back 28

If the infant is found to have PKU, a diet low in phenylalanine is begun soon after birth. Breastfeeding or partial breastfeeding may be possible for some infants if the phenylalanine levels are monitored carefully and remain within acceptable limits (Kirby, 1999). Many affected children have some intellectual impairment. Successful management and outcome is largely dependent on early identification of the condition, modifying the diet, and compliance with the treatment regimen throughout the entire life cycle.

Front 29

Galactosemia

Back 29

Caused by a deficiency of the enzyme galactose-1-phosphate uridyltransferase, results in the inability to convert galactose to glucose.

Front 30

How is galactosemia tested, the symptoms, and treatment?

Back 30

Galactosemia can be detected by measuring the blood levels of galactose in the urine of newborns suspected of having the disease who have ingested formula containing galactose. Early symptoms are vomiting, weight loss, and CNS symptoms, including poor feeding, drowsiness, and seizures. If the disorder goes untreated, the galactose levels will continue to increase and the affected infant will show failure to thrive, mental retardation, cataracts, jaundice, hepatomegaly, and cirrhosis of the liver, with death possibly occurring in the first month of life. Therapy consists of eliminating lactose from the diet; this condition precludes breastfeeding since lactose is present in breast milk.

Front 31

What does the the course of normal labor consist of?

Back 31

It consists of (1) regular progression of uterine contractions, (2) effacement and progressive dilation of the cervix, and (3) progress in descent of the presenting part.

Front 32

The four stages of labor

Back 32

1. The first stage of labor is considered to last from the onset of regular uterine contractions to full dilation of the cervix.
2. The second stage of labor lasts from the time the cervix is fully dilated to the birth of the fetus.
3. The third stage of labor lasts from the birth of the fetus until the placenta is delivered.
4. The fourth stage of labor arbitrarily lasts about 2 hours after delivery of the placenta. It is the period of immediate recovery, when homeostasis is reestablished.

Front 33

What are the 3 phases of the first stage of labor?

Back 33

• The latent phase (up to 3 cm of dilation)
• The active phase (4 to 7 cm of dilation)
• The transition phase (8 to 10 cm of dilation).

Front 34

What happens during the latent phase of the first stage of labor?

Back 34

During the latent phase, there is more progress in effacement of the cervix and little increase in descent. up to 3 cm of dilation.

Front 35

The active phase of the first stage of labor

Back 35

4 to 7 cm of dilation

Front 36

The transition phase of the first stage of labor

Back 36

8 to 10 cm of dilation

Front 37

The second stage of labor

Back 37

lasts from the time the cervix is fully dilated to the birth of the fetus. The second stage takes an average of 20 minutes for a multiparous woman and 50 minutes for a nulliparous woman. Labor of up to 2 hours has been considered within the normal range for the second stage, but there can be significant variations.

Front 38

The latent and active phases of second-stage labor

Back 38

The latent phase is a period that begins about the time of complete dilation of the uterus when the contractions are weak or not noticeable and the woman is not feeling the urge to push, is resting, or is exerting only small bearing-down efforts with contractions. The active phase is a period when contractions resume, the woman is making strong bearing-down efforts, and the fetal station is advancing.

Front 39

The third stage of labor

Back 39

The third stage of labor lasts from the birth of the fetus until the placenta is delivered. The placenta normally separates with the third or fourth strong uterine contraction after the infant has been born. After it has separated, the placenta can be delivered with the next uterine contraction. The duration of the third stage may be as short as 3 to 5 minutes, although up to 1 hour is considered within normal limits. The risk of hemorrhage increases as the length of the third stage increases.

Front 40

The fourth stage of labor

Back 40

The fourth stage of labor arbitrarily lasts about 2 hours after delivery of the placenta. It is the period of immediate recovery, when homeostasis is reestablished. It is an important period of observation for complications, such as abnormal bleeding.

Front 41

What characteristics are used to describe a uterine contraction?

Back 41

• Frequency—How often uterine contractions occur; the time that elapses from the beginning of one contraction to the beginning of the next
• Intensity—The strength of a contraction at its peak
• Duration—The time that elapses between the onset and the end of a contraction
• Resting tone—The tension in the uterine muscle between contractions

Front 42

When does Rh incompatibility occur?

Back 42

Occurs when an RhD-negative mother has an RhD-positive fetus who inherits the dominant Rh-positive gene from the father.

Front 43

When does Rh incompatibility occur?

Back 43

If the mother is Rh-negative, and the father is Rh-positive and homozygous for the Rh factor, all the offspring will be Rh-positive. If the father is heterozygous for the factor, there is a 50% chance that each infant born of the union will be Rh-positive and a 50% chance that each will be Rh-negative.

Front 44

How is Rh incompatibility treated?

Back 44

With RhoGam, intrauterine transfusion, or exchange transfusion.

Front 45

ABO incompatibility

Back 45

It occurs if the fetal blood type is A, B, or AB and the maternal type is O. It occurs rarely in infants with type B blood born to mothers with type A blood. The incompatibility arises because naturally occurring anti-A and anti-B antibodies are transferred across the placenta to the fetus.

Front 46

What is the treatment for ABO incompatibility?

Back 46

Any resulting hyperbilirubinemia usually can be treated with phototherapy. Exchange transfusions are required only occasionally. Although ABO incompatibility is a common cause of hyperbilirubinemia, it rarely precipitates significant anemia resulting from the hemolysis of RBCs.

Front 47

What is the most common and fastest-spreading STI in American women?

Back 47

Chlamydia

Front 48

What does Chlamydia lead to?

Back 48

Untreated infection often leads to acute salpingitis or pelvic inflammatory disease.

Front 49

What are some symptoms of Gonorrhea?

Back 49

Women are often asymptomatic, with one third of infections in adolescent women going unnoticed. When symptoms are present, they are often less specific than the symptoms in men. Women may have a purulent endocervical discharge, but discharge is usually minimal or absent. Menstrual irregularities may be the initial symptom, or women may complain of pain: chronic or acute severe pelvic or lower abdominal pain or longer, more painful menses. Infrequently, dysuria, vague abdominal pain, or low backache prompts a woman to seek care.

Front 50

How is primary syphilis characterized?

Back 50

It is characterized by a primary lesion, the chancre, that appears 5 to 90 days after infection. This lesion often begins as a painless papule at the site of inoculation and then erodes to form a nontender, shallow, indurated, clean ulcer several millimeters to centimeters in size.

Front 51

How is secondary syphilis characterized?

Back 51

It is characterized by a widespread, symmetric, maculopapular rash on the palms and soles and generalized lymphadenopathy. The infected individual also may experience fever, headache, and malaise.

Front 52

What happens in the later phases of Syphilis if left untreated?

Back 52

Left untreated, about one third of these women will develop tertiary syphilis. Neurologic, cardiovascular, musculoskeletal, or multiorgan system complications can develop in the third stage.

Front 53

Pelvic inflammatory disease (PID)

Back 53

It's an infectious process that most commonly involves the uterine tubes, causing salpingitis; the uterus, causing endometritis; and, more rarely, the ovaries and peritoneal surfaces. Multiple organisms have been found to cause PID; most cases are associated with more than one organism.

Front 54

What is the single most frequent serious infection encountered by women?

Back 54

PID

Front 55

Human papillomavirus (HPV)

Back 55

Human papillomavirus (HPV) infection, previously named genital or venereal warts, is a sexually transmitted infection that was first described in 25 AD and is now the most common viral STI seen in ambulatory health care settings.

Front 56

Group B Streptococcus

Back 56

Until recently GBS has been the most common cause of neonatal sepsis and meningitis in the United States; however, antepartum maternal screening and administration of penicillin has significantly decreased the incidence of GBS.

Usually resulting from vertical transmission from the birth canal, early-onset disease results in a respiratory illness that mimics the symptoms of severe respiratory distress syndrome. The infant may rapidly develop septic shock, which has a significant mortality rate.

Eighty-five percent of infants with late-onset GBS have meningitis; this population has a mortality rate of 0% to 23%. Fifty percent of the survivors develop neurologic damage.