Nursing practice questions with comprehensive rationales
NurseDive Free Nursing Practice Question
A 3-year-old child with a history of recurrent respiratory infections, poor weight gain, and salty-tasting skin is being evaluated for cystic fibrosis (CF). The healthcare provider suspects CF and orders a diagnostic test. Which of the following diagnostic tests is the gold standard for confirming the diagnosis of CF?
A. Genetic testing for CFTR mutations
Genetic testing for CFTR mutations is incorrect as the primary diagnostic tool. While genetic testing can identify specific CF mutations and is useful for screening or confirming atypical cases, it is not considered the first-line gold standard for diagnosis.
B. Sweat chloride test
Sweat chloride test is correct. The sweat chloride test measures the concentration of chloride in sweat, which is abnormally elevated in individuals with cystic fibrosis due to defective CFTR channels. A chloride concentration ≥60 mmol/L on two separate occasions confirms the diagnosis. It remains the gold standard diagnostic test for CF in children.
C. Chest x-ray
Chest x-ray is incorrect because it is not diagnostic for CF. Although chest x-rays may show structural lung changes such as hyperinflation or bronchiectasis in advanced disease, they cannot confirm CF on their own.
D. Pulmonary function tests (PFTS)
Pulmonary function tests (PFTs) are incorrect for initial diagnosis in young children. PFTs assess lung function and disease progression but are not reliable for confirming CF, especially in a 3-year-old who may not be able to perform the maneuvers required.
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Full Explanation
A. Genetic testing for CFTR mutations is incorrect as the primary diagnostic tool. While genetic testing can identify specific CF mutations and is useful for screening or confirming atypical cases, it is not considered the first-line gold standard for diagnosis.
B. Sweat chloride test is correct. The sweat chloride test measures the concentration of chloride in sweat, which is abnormally elevated in individuals with cystic fibrosis due to defective CFTR channels. A chloride concentration ≥60 mmol/L on two separate occasions confirms the diagnosis. It remains the gold standard diagnostic test for CF in children.
C. Chest x-ray is incorrect because it is not diagnostic for CF. Although chest x-rays may show structural lung changes such as hyperinflation or bronchiectasis in advanced disease, they cannot confirm CF on their own.
D. Pulmonary function tests (PFTs) are incorrect for initial diagnosis in young children. PFTs assess lung function and disease progression but are not reliable for confirming CF, especially in a 3-year-old who may not be able to perform the maneuvers required.
Similar Questions
A 5-year-old child with cystic fibrosis (CF) is being seen for a follow-up visit. The parents report that the child has difficulty gaining weight despite a high- calorie diet and frequently experiences loose, fatty stools. The healthcare provider prescribes pancreatic enzyme replacement therapy (PERT) to assist with digestion. Which of the following statements best explains why children with CF require digestive enzymes?
A. Pancreatic enzyme replacement is only required when children develop diabetes, a common complication of CF
Pancreatic enzyme replacement therapy (PERT) is not tied to the development of diabetes. While CF-related diabetes can occur due to progressive pancreatic damage, enzyme therapy is required much earlier to address malabsorption caused by blocked pancreatic ducts. Waiting for diabetes to develop would allow continued nutrient deficiencies, poor weight gain, and fat-soluble vitamin deficiencies (A, D, E, K).
B. Digestive enzymes are needed to break down fat, which children with CF can digest more efficiently than carbohydrates
Children with CF do not digest fats more efficiently than carbohydrates. In fact, fat digestion is particularly impaired because pancreatic lipase is insufficient due to duct obstruction. Proteins and carbohydrates are also affected to a lesser extent. PERT provides a mix of lipase, amylase, and protease to compensate for this deficiency and ensure adequate nutrient absorption.
C. Children with CF have an overproduction of digestive enzymes, leading to malabsorption
CF does not cause an overproduction of digestive enzymes. On the contrary, thick mucus blocks pancreatic ducts, preventing enzymes from reaching the intestines. This blockage leads to enzyme deficiency in the gastrointestinal tract, resulting in malabsorption, steatorrhea (fatty stools), abdominal bloating, and poor growth.
D. CF causes thickened mucus that obstructs the pancreas, preventing the release of digestive enzymes
In CF, mutations in the CFTR gene lead to thick, sticky mucus production in multiple organs, including the pancreas. This mucus obstructs the pancreatic ducts, preventing digestive enzymes such as lipase, amylase, and protease from reaching the small intestine. Without these enzymes, fats, proteins, and carbohydrates are incompletely digested, causing nutrient malabsorption, fatty stools, and poor weight gain. PERT replaces the missing enzymes, allowing proper digestion and absorption of nutrients, improving growth, and reducing gastrointestinal symptoms. Regular dosing with meals and snacks is essential to optimize nutrient absorption and support normal growth and development in children with CF.
Full Explanation
A. Pancreatic enzyme replacement therapy (PERT) is not tied to the development of diabetes. While CF-related diabetes can occur due to progressive pancreatic damage, enzyme therapy is required much earlier to address malabsorption caused by blocked pancreatic ducts. Waiting for diabetes to develop would allow continued nutrient deficiencies, poor weight gain, and fat-soluble vitamin deficiencies (A, D, E, K).
B. Children with CF do not digest fats more efficiently than carbohydrates. In fact, fat digestion is particularly impaired because pancreatic lipase is insufficient due to duct obstruction. Proteins and carbohydrates are also affected to a lesser extent. PERT provides a mix of lipase, amylase, and protease to compensate for this deficiency and ensure adequate nutrient absorption.
C. CF does not cause an overproduction of digestive enzymes. On the contrary, thick mucus blocks pancreatic ducts, preventing enzymes from reaching the intestines. This blockage leads to enzyme deficiency in the gastrointestinal tract, resulting in malabsorption, steatorrhea (fatty stools), abdominal bloating, and poor growth.
D. In CF, mutations in the CFTR gene lead to thick, sticky mucus production in multiple organs, including the pancreas. This mucus obstructs the pancreatic ducts, preventing digestive enzymes such as lipase, amylase, and protease from reaching the small intestine. Without these enzymes, fats, proteins, and carbohydrates are incompletely digested, causing nutrient malabsorption, fatty stools, and poor weight gain. PERT replaces the missing enzymes, allowing proper digestion and absorption of nutrients, improving growth, and reducing gastrointestinal symptoms. Regular dosing with meals and snacks is essential to optimize nutrient absorption and support normal growth and development in children with CF.
A 5.6 kg patient is receiving digoxin by mouth every 8 hours. The safe dose is 0.03-0.06 mg/kg/day. What is the maximum safe dose for this patient? (Round to the nearest hundredth.)
Full Explanation
Given:
- Patient weight = 5.6 kg
- Safe dose = 0.03–0.06 mg/kg/day
Step 1: Use the formula for maximum safe dose
Maximum dose = Weight × Maximum mg/kg/day
Step 2: Substitute the values
Maximum dose = 5.6 × 0.06
Step 3: Calculate
Maximum dose = 0.336 mg/day
Step 4: Round to the nearest hundredth
Maximum dose = 0.34 mg/day
Screening at 24 weeks of gestation reveals that a pregnant woman has gestational diabetes mellitus (GDM). In planning her care, the nurse and the woman mutually agree that an expected outcome is to prevent injury to the fetus as a result of GDM. The nurse identifies that the fetus is at greatest risk for
A. macrosomia.
Macrosomia, defined as a birth weight greater than 4,000–4,500 grams, is the most common fetal complication associated with gestational diabetes. Hyperglycemia in the mother leads to increased glucose transfer across the placenta, stimulating fetal pancreatic insulin production. Fetal hyperinsulinemia acts as a growth-promoting hormone, resulting in excessive fat and muscle deposition and ultimately large-for-gestational-age infants. Macrosomia increases the risk of birth injuries such as shoulder dystocia, clavicle fractures, and the need for cesarean delivery.
B. preterm birth.
Preterm birth is not the primary risk associated with GDM. While poorly controlled diabetes can contribute to preterm labor, it is less common than macrosomia. The main concern in GDM is excessive fetal growth, not premature delivery.
C. low birth weight
Low birth weight is not typically associated with gestational diabetes. In fact, infants of mothers with poorly controlled GDM are often larger than average, not smaller, due to fetal hyperinsulinemia and increased nutrient availability.
D. congenital anomalies of the central nervous system.
Congenital anomalies, particularly neural tube defects or central nervous system defects, are primarily associated with pregestational diabetes rather than GDM. Gestational diabetes develops later in pregnancy (usually after 24 weeks) when organogenesis has largely occurred, so the risk for major congenital anomalies is minimal.
Full Explanation
A. Macrosomia, defined as a birth weight greater than 4,000–4,500 grams, is the most common fetal complication associated with gestational diabetes. Hyperglycemia in the mother leads to increased glucose transfer across the placenta, stimulating fetal pancreatic insulin production. Fetal hyperinsulinemia acts as a growth-promoting hormone, resulting in excessive fat and muscle deposition and ultimately large-for-gestational-age infants. Macrosomia increases the risk of birth injuries such as shoulder dystocia, clavicle fractures, and the need for cesarean delivery.
B. Preterm birth is not the primary risk associated with GDM. While poorly controlled diabetes can contribute to preterm labor, it is less common than macrosomia. The main concern in GDM is excessive fetal growth, not premature delivery.
C. Low birth weight is not typically associated with gestational diabetes. In fact, infants of mothers with poorly controlled GDM are often larger than average, not smaller, due to fetal hyperinsulinemia and increased nutrient availability.
D. Congenital anomalies, particularly neural tube defects or central nervous system defects, are primarily associated with pregestational diabetes rather than GDM. Gestational diabetes develops later in pregnancy (usually after 24 weeks) when organogenesis has largely occurred, so the risk for major congenital anomalies is minimal.