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NurseDive Free Nursing Practice Question
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.
This question is an excerpt from Nurse Dive's nursing test bank - Ati Demsn 650 Pediatrics Proctored Exam. Take the full exam now
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.
Similar Questions
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.
A 12-week pregnant client presents for a routine checkup. She reports no vaginal bleeding or cramping, but her last fetal heartbeat detected on ultrasound is absent. The cervix is closed, and the client feels no fetal movement. Which type of miscarriage does the nurse suspect?
A. Threatened miscarriage
A threatened miscarriage is characterized by vaginal bleeding, mild cramping, and a closed cervix, but the fetus is still viable with a detectable heartbeat. In this case, the fetal heartbeat is absent, making a threatened miscarriage unlikely.
B. Incomplete miscarriage
An incomplete miscarriage occurs when some products of conception have been expelled while others remain in the uterus. It is usually accompanied by heavy bleeding, cramping, and an open cervix. This client has a closed cervix and no bleeding, ruling out an incomplete miscarriage.
C. Missed miscarriage
A missed miscarriage occurs when the fetus has died in utero but has not been expelled. The client may have no symptoms—no bleeding or cramping—and the cervix remains closed. Ultrasound confirms the absence of fetal cardiac activity, which matches this presentation. Missed miscarriages often require medical or surgical management to prevent complications such as infection or coagulopathy.
D. Inevitable miscarriage
An inevitable miscarriage is indicated by vaginal bleeding, cramping, and cervical dilation, suggesting that miscarriage is in progress and cannot be prevented. Since this client has a closed cervix and no active bleeding, an inevitable miscarriage is unlikely.
Full Explanation
A. A threatened miscarriage is characterized by vaginal bleeding, mild cramping, and a closed cervix, but the fetus is still viable with a detectable heartbeat. In this case, the fetal heartbeat is absent, making a threatened miscarriage unlikely.
B. An incomplete miscarriage occurs when some products of conception have been expelled while others remain in the uterus. It is usually accompanied by heavy bleeding, cramping, and an open cervix. This client has a closed cervix and no bleeding, ruling out an incomplete miscarriage.
C. A missed miscarriage occurs when the fetus has died in utero but has not been expelled. The client may have no symptoms—no bleeding or cramping—and the cervix remains closed. Ultrasound confirms the absence of fetal cardiac activity, which matches this presentation. Missed miscarriages often require medical or surgical management to prevent complications such as infection or coagulopathy.
D. An inevitable miscarriage is indicated by vaginal bleeding, cramping, and cervical dilation, suggesting that miscarriage is in progress and cannot be prevented. Since this client has a closed cervix and no active bleeding, an inevitable miscarriage is unlikely.