AIM β’ KMU Exam Reasoning
KMU Past Paper Practice
Topic 9 β Atelectasis, Acute Lung Injury and Respiratory Distress Syndrome
3rd Year MBBS β’ 20 A-type Single Best Answer MCQs
MCQ 1
Question:
A 58-year-old man has complete obstruction of a segmental bronchus by an intraluminal lesion. The distal lung gradually loses its air without accumulation of pleural fluid. Which process is responsible for the resulting atelectasis?
Options:
Fibrotic restriction of lung expansion
Inflammatory destruction of alveolar septa
Removal of distal gas into the bloodstream
Leakage of protein-rich fluid into alveoli
External compression of the affected segment
Correct Answer: Removal of distal gas into the bloodstream
Explanation: Complete bronchial obstruction prevents replacement of distal air; continued absorption of that gas into blood makes the affected alveoli progressively collapse.
MCQ 2
Question:
Two patients develop lung collapse. One has an obstructed bronchus, while the other has a large collection of fluid in the pleural cavity. Which feature best distinguishes the mechanism in the second patient?
Options:
The lung is compressed despite an open airway
Distal gas is absorbed after airway blockage
Scar tissue prevents subsequent lung expansion
Neutrophils damage the alveolar-capillary membrane
Type II pneumocyte injury reduces surfactant activity
Correct Answer: The lung is compressed despite an open airway
Explanation: Pleural fluid produces compression atelectasis by exerting pressure from outside; unlike resorption atelectasis, bronchial obstruction is not required.
MCQ 3
Question:
A patient has chronic fibrotic thickening involving the lung and pleura. Imaging demonstrates persistent reduction in expansion of the affected region. Which feature makes this form of atelectasis different from collapse caused by a temporary bronchial obstruction?
Options:
Alveolar fluid is rich in plasma proteins
Distal air is progressively absorbed
Pleural pressure directly compresses alveoli
Scarring mechanically limits re-expansion
Surfactant production is temporarily reduced
Correct Answer: Scarring mechanically limits re-expansion
Explanation: Contraction atelectasis results from fibrosis of lung or pleura; the scar physically restricts expansion rather than merely removing air from patent alveoli.
MCQ 4
Question:
A patient develops widespread acute pulmonary injury. Despite ventilation, many alveoli become unstable and collapse. Damage to which cell population contributes most directly to the surfactant abnormality responsible for this component of the disease?
Options:
Alveolar macrophages
Pulmonary neutrophils
Capillary endothelial cells
Bronchial goblet cells
Type II pneumocytes
Correct Answer: Type II pneumocytes
Explanation: Type II pneumocytes produce surfactant. Their injury in ARDS reduces surfactant activity, increasing alveolar instability and contributing to collapse.
MCQ 5
Question:
A 47-year-old patient develops severe acute respiratory failure after a major inflammatory insult. Histology shows endothelial and epithelial injury with leakage of protein-rich fluid into alveoli. Which subsequent change most directly makes the lungs difficult to expand?
Options:
Loss of bronchial cartilage support
Edema with alveolar collapse
Excessive removal of alveolar fluid
Dilatation of conducting bronchi
Reduction in pulmonary perfusion
Correct Answer: Edema with alveolar collapse
Explanation: Alveolar edema together with surfactant dysfunction and collapse makes the ARDS lung stiff and poorly compliant, increasing the pressure needed for expansion.
MCQ 6
Question:
Microscopy from the lung of a patient in the acute phase of ARDS shows capillary congestion, interstitial edema and intra-alveolar fluid. Which additional finding would most strongly support the characteristic pathological pattern?
Options:
Marked bronchial gland enlargement
Destruction of alveolar septal walls
Dense pleural collagen deposition
Eosinophilic lining of damaged alveoli
Permanent dilatation of bronchioles
Correct Answer: Eosinophilic lining of damaged alveoli
Explanation: Hyaline membranes appear as eosinophilic material lining injured alveoli and are a characteristic morphological feature of diffuse alveolar damage.
MCQ 7
Question:
A patient with ARDS survives the initial exudative injury. Several days later, alveolar epithelial regeneration is evident. Which finding represents an appropriate reparative response rather than continuing acute injury?
Options:
Proliferation of type II pneumocytes
Increasing endothelial permeability
Accumulation of intra-alveolar edema
Continued epithelial cell necrosis
Further neutrophil-mediated tissue injury
Correct Answer: Proliferation of type II pneumocytes
Explanation: Surviving type II pneumocytes proliferate during recovery to restore the damaged alveolar epithelial lining; the other changes indicate ongoing injury.
MCQ 8
Question:
Two patients recover from the acute phase of ARDS. One regains near-normal pulmonary function, whereas the other has persistent stiff lungs. Which pathological event most likely occurred in the second patient?
Options:
Complete clearance of alveolar edema
Restoration of surfactant activity
Resolution of epithelial inflammation
Re-expansion of collapsed alveoli
Organization of injury with fibrosis
Correct Answer: Organization of injury with fibrosis
Explanation: Organization of the inflammatory exudate with interstitial fibrosis can follow ARDS and leaves the lung persistently less compliant.
MCQ 9
Question:
In experimental acute lung injury, activated neutrophils are prevented from releasing their major damaging products. Which component of ARDS pathogenesis would be most directly reduced?
Options:
Fibrotic contraction of the pleura
Protease and oxidant-mediated tissue injury
Absorption of air behind an obstruction
Mechanical compression by pleural fluid
Primary developmental surfactant deficiency
Correct Answer: Protease and oxidant-mediated tissue injury
Explanation: Activated neutrophils amplify ARDS by releasing proteases and reactive oxygen species that injure alveolar epithelium and pulmonary endothelium.
MCQ 10
Question:
An adult with severe ARDS and a premature newborn with respiratory distress both have unstable alveoli. Which statement best distinguishes the role of surfactant in these two conditions?
Options:
Surfactant excess initiates both disorders
Surfactant is unaffected in both disorders
Deficiency develops only after pleural compression
Dysfunction is secondary in ARDS but primary in neonatal RDS
Deficiency is caused by bronchial obstruction in both
Correct Answer: Dysfunction is secondary in ARDS but primary in neonatal RDS
Explanation: Adult ARDS begins with acute alveolar-capillary injury and secondary surfactant impairment; neonatal RDS centers on inadequate surfactant production in immature lungs.
MCQ 11
Question:
Two newborns are delivered on the same day. One is markedly premature and the other is full term. The premature infant develops progressive respiratory difficulty soon after birth. Which developmental factor best explains the difference in risk?
Options:
Immature lungs have greater pulmonary fibrosis
Premature lungs contain excess pleural fluid
Surfactant production increases with fetal maturation
Prematurity produces fixed bronchial obstruction
Pulmonary capillary injury accompanies normal delivery
Correct Answer: Surfactant production increases with fetal maturation
Explanation: Surfactant production rises as the fetal lungs mature, so premature delivery may occur before sufficient surfactant is available to maintain alveolar stability.
MCQ 12
Question:
A premature newborn develops tachypnea and marked chest retractions shortly after birth. Which physiological sequence best explains the increased respiratory effort?
Options:
Reduced surfactant β higher surface tension β lower compliance
Increased surfactant β lower surface tension β lower compliance
Pleural compression β higher surfactant β alveolar collapse
Airway obstruction β fibrosis β reduced lung expansion
Capillary injury β reduced permeability β pulmonary edema
Correct Answer: Reduced surfactant β higher surface tension β lower compliance
Explanation: Surfactant deficiency increases alveolar surface tension, promotes collapse and reduces compliance, so greater inspiratory effort is required to expand the lungs.
MCQ 13
Question:
A premature infant is tachypneic with nasal flaring and intercostal retractions. The infant begins grunting during expiration. Which change is the infant attempting to achieve through this maneuver?
Options:
Lower pulmonary capillary permeability
Greater clearance of bronchial secretions
Faster production of pulmonary surfactant
Higher pressure at the end of expiration
Reduced pulmonary capillary blood flow
Correct Answer: Higher pressure at the end of expiration
Explanation: Expiratory grunting helps maintain positive end-expiratory pressure, limiting collapse of surfactant-deficient alveoli between breaths.
MCQ 14
Question:
A 31-week newborn develops respiratory distress. Continuous bedside monitoring shows reduced oxygen saturation, but the clinical team also needs to assess ventilation and acid-base disturbance. Which investigation provides the required additional information?
Options:
Repeat pulse oximetry alone
Chest radiographic examination
Pleural fluid examination
Bronchoscopic airway examination
Blood gas analysis
Correct Answer: Blood gas analysis
Explanation: Blood gas analysis assesses oxygenation together with carbon dioxide and acid-base status, providing information that pulse oximetry alone cannot supply.
MCQ 15
Question:
A premature newborn has respiratory distress and diffuse reduction in lung aeration. Chest radiography shows a fine reticulogranular appearance. Which additional radiological finding would support the same underlying process?
Options:
Air bronchograms within poorly aerated lungs
A solitary thick-walled apical cavity
Localized pleural calcification
Marked unilateral lung hyperinflation
Multiple cavitating pulmonary lesions
Correct Answer: Air bronchograms within poorly aerated lungs
Explanation: Neonatal RDS can produce diffuse fine reticulogranular or ground-glass opacity with air bronchograms because the alveoli are poorly expanded while larger airways remain air filled.
MCQ 16
Question:
A preterm infant with surfactant deficiency remains spontaneously breathing but has recurrent end-expiratory alveolar collapse. Which treatment principle most directly counteracts this mechanical problem without replacing surfactant itself?
Options:
Reducing pulmonary blood flow
Increasing bronchial mucus clearance
Maintaining continuous positive airway pressure
Removing fluid from the pleural cavity
Promoting fibrotic support of alveoli
Correct Answer: Maintaining continuous positive airway pressure
Explanation: CPAP provides positive pressure that helps keep unstable alveoli open at end-expiration, directly reducing repeated collapse.
MCQ 17
Question:
A premature infant receives exogenous surfactant. Soon afterward, less inspiratory pressure is required to expand the lungs. Which physiological change best explains this response?
Options:
Increased pulmonary vascular permeability
Reduced pulmonary capillary perfusion
Increased fibrous support of alveolar walls
Reduced surface tension with improved compliance
Increased resistance in conducting airways
Correct Answer: Reduced surface tension with improved compliance
Explanation: Exogenous surfactant lowers alveolar surface tension, stabilizes alveoli and improves compliance, so less pressure is required to inflate the lungs.
MCQ 18
Question:
A preterm newborn with respiratory distress is receiving supplemental oxygen but develops worsening respiratory effort and inadequate gas exchange. Which management step is most appropriate when basic support is no longer sufficient to maintain ventilation?
Options:
Pleural drainage for all affected infants
Mechanical ventilatory support when required
Bronchoscopy to remove distal alveolar fluid
Restriction of respiratory support to oxygen alone
Treatment directed at pulmonary fibrosis
Correct Answer: Mechanical ventilatory support when required
Explanation: Severe neonatal respiratory failure may require mechanical ventilation when adequate gas exchange cannot be maintained with less intensive respiratory support.
MCQ 19
Question:
A premature newborn with respiratory distress is placed in a thermally controlled environment while respiratory support is arranged. What is the main rationale for this component of supportive management?
Options:
It directly stimulates mature surfactant synthesis
It reverses established alveolar fibrosis
It removes protein-rich alveolar edema
It mechanically increases airway pressure
It limits unnecessary metabolic and oxygen demand
Correct Answer: It limits unnecessary metabolic and oxygen demand
Explanation: Maintaining thermal stability is part of supportive neonatal care because unnecessary heat loss increases metabolic activity and oxygen requirements.
MCQ 20
Question:
A student reviews three patients: one has bronchial obstruction with distal lung collapse, another has inflammatory alveolar-capillary injury with protein-rich edema, and a third is a premature newborn with unstable alveoli. Which sequence correctly matches the principal mechanism in each patient?
Options:
Fibrosis β hydrostatic edema β bronchial obstruction
Pleural compression β fibrosis β capillary obstruction
Distal gas absorption β permeability injury β surfactant deficiency
Surfactant deficiency β airway obstruction β pleural compression
Permeability injury β distal gas absorption β pulmonary fibrosis
Correct Answer: Distal gas absorption β permeability injury β surfactant deficiency
Explanation: Obstructive atelectasis follows absorption of trapped distal gas, ARDS centers on permeability injury, and neonatal RDS primarily results from inadequate surfactant.
Assessment structure and topic coverage follow the supplied KMU Past Paper Practice specification. :contentReference[oaicite:0]{index=0}