Nursing practice questions with comprehensive rationales
NurseDive Free Nursing Practice Question
A 10-year-old child with a known history of asthma presents to the clinic with increased coughing, wheezing, and chest tightness, especially at night. The nurse explains that these symptoms are related to the underlying pathophysiology of asthma. Which of the following best describes the primary pathophysiologic processes occurring during an asthma exacerbation?
A. Collapse of alveoli due to surfactant deficiency and impaired gas exchange
Alveolar collapse (atelectasis) due to surfactant deficiency is typically seen in neonatal respiratory distress syndrome, not asthma. Asthma primarily affects the airways, not alveolar surfactant production.
B. Bronchial smooth muscle relaxation and increased surfactant production
In asthma, bronchial smooth muscle constriction occurs, not relaxation. Surfactant production is not a central factor in asthma pathophysiology.
C. Chronic airway inflammation, bronchoconstriction, and increased mucus production
These features lead to edema and hyperresponsiveness, contraction of smooth muscle around the bronchi and bronchioles, and mucus accumulation, all contributing to the child’s symptoms.
D. Acute upper airway infection leading to mucus obstruction in the sinuses
While upper respiratory infections can trigger asthma exacerbations, sinus obstruction itself is not the primary pathophysiologic process in asthma. The key changes occur in the lower airways.
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. Alveolar collapse (atelectasis) due to surfactant deficiency is typically seen in neonatal respiratory distress syndrome, not asthma. Asthma primarily affects the airways, not alveolar surfactant production.
B. In asthma, bronchial smooth muscle constriction occurs, not relaxation. Surfactant production is not a central factor in asthma pathophysiology.
C. These features lead to edema and hyperresponsiveness, contraction of smooth muscle around the bronchi and bronchioles, and mucus accumulation, all contributing to the child’s symptoms.
D. While upper respiratory infections can trigger asthma exacerbations, sinus obstruction itself is not the primary pathophysiologic process in asthma. The key changes occur in the lower airways.
Similar Questions
A newborn is delivered vaginally after a prolonged second stage of labor with the use of forceps. Upon assessment, the nurse notes weak movement of the left arm, absent Moro reflex on that side, and intact grasp reflex. Which birth injury should the nurse suspect?
A. Erb's palsy
The combination of weak arm movement, absent Moro reflex, and intact grasp reflex directly points to an upper brachial plexus injury, consistent with Erb’s palsy. Immediate management includes supportive care, gentle range-of-motion exercises, and referral to a pediatric neurologist or physical therapist. Early intervention improves functional outcomes and reduces long-term disability.
B. Facial nerve injury
Caput succedaneum is diffuse edema of the scalp caused by pressure during delivery, often crossing suture lines. It is benign, self-limiting, and does not affect limb movement or reflexes. The infant’s motor deficits are not explained by caput succedaneum.
C. Cephalohematoma
Cephalohematoma is a localized subperiosteal blood collection, typically limited by suture lines. It presents as a firm scalp swelling, sometimes with jaundice as a complication. Cephalohematoma does not cause limb weakness or absent reflexes, so it is inconsistent with the findings in this case.
D. Caput succedaneum
Facial nerve injury during birth, often due to traction or forceps application on the face, manifests as facial asymmetry, inability to close the eyelid, drooping of the mouth, or absent nasolabial fold. It does not affect arm movement or the Moro reflex, so it cannot account for the infant’s symptoms.
Full Explanation
A. The combination of weak arm movement, absent Moro reflex, and intact grasp reflex directly points to an upper brachial plexus injury, consistent with Erb’s palsy. Immediate management includes supportive care, gentle range-of-motion exercises, and referral to a pediatric neurologist or physical therapist. Early intervention improves functional outcomes and reduces long-term disability.
B. Caput succedaneum is diffuse edema of the scalp caused by pressure during delivery, often crossing suture lines. It is benign, self-limiting, and does not affect limb movement or reflexes. The infant’s motor deficits are not explained by caput succedaneum.
C. Cephalohematoma is a localized subperiosteal blood collection, typically limited by suture lines. It presents as a firm scalp swelling, sometimes with jaundice as a complication. Cephalohematoma does not cause limb weakness or absent reflexes, so it is inconsistent with the findings in this case.
D. Facial nerve injury during birth, often due to traction or forceps application on the face, manifests as facial asymmetry, inability to close the eyelid, drooping of the mouth, or absent nasolabial fold. It does not affect arm movement or the Moro reflex, so it cannot account for the infant’s symptoms.
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.
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.
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.