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BRS PHYSIOLOGY: RESPIRATORY EXAM QUESTIONS WITH COMPLETE VERIFIED SOLUTIONS GRADED A++
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BRS PHYSIOLOGY
BRS PHYSIOLOGY: RESPIRATORY EXAM QUESTIONS WITH COMPLETE VERIFIED SOLUTIONS GRADED A++
1. The answer is E [I A 4, 5, B 2, 3, 5]. Residual volume (RV) cannot be measured by spirometry. Therefore, any lung volume or capacity that includes the RV cannot be measured by spirometry. Measurements that in...
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BRS PHYSIOLOGY: RESPIRATORY EXAM QUESTIONS WITH
COMPLETE VERIFIED SOLUTIONS GRADED A++
1. The answer is E [I A 4, 5, B 2, 3, 5]. Residual volume (RV) cannot be measured
by spirometry. Therefore, any lung volume or capacity that includes the RV
cannot be measured by spirometry. Measurements that include RV are functional
residual capacity (FRC) and total lung capacity (TLC). Vital capacity (VC) does not
include RV and is, therefore, measurable by spirometry. Physiologic dead space
is not measurable by spirometry and requires sampling of arterial PCO2 and
expired CO2.
1. Which of the following lung volumes or capacities can be measured by spirometry?
(A) Functional residual capacity (FRC)
(B) Physiologic dead space
(C) Residual volume (RV)
(D) Total lung capacity (TLC)
(E) Vital capacity (VC)
2. The answer is B [II D 2]. Neonatal respiratory distress syndrome is caused by
lack of adequate surfactant in the immature lung. Surfactant appears between the
24th and the 35th gestational week. In the absence of surfactant, the surface
tension of the small alveoli is too high. When the pressure on the small alveoli is
too high (P = 2T/r), the small alveoli collapse into larger alveoli. There is
decreased gas exchange with the larger, collapsed alveoli, and V/Q mismatch,
,hypoxemia, and cyanosis occur. The lack of surfactant also decreases lung
compliance, making it harder to inflate the lungs, increasing the work of
breathing, and producing dyspnea. Generally, lecithin:sphingomyelin ratios
greater than 2:1 signify mature levels of surfactant.
2. An infant born prematurely in gestational week 25 has neonatal respiratory distress
syndrome. Which of the following would be expected in this infant?
(A) Arterial PO2 of 100 mm Hg
(B) Collapse of the small alveoli
(C) Increased lung compliance
(D) Normal breathing rate
(E) Lecithin:sphingomyelin ratio of greater than 2:1 in amniotic fluid
3. The answer is B [VI C]. Pulmonary blood flow is controlled locally by the PO2 of
alveolar
air. Hypoxia causes pulmonary vasoconstriction and thereby shunts blood away
from unventilated areas of the lung, where it would be wasted. In the coronary
circulation,
hypoxemia causes vasodilation. The cerebral, muscle, and skin circulations are
not controlled directly by PO2.
3. In which vascular bed does hypoxia cause vasoconstriction?
(A) Coronary
(B) Pulmonary
(C) Cerebral
, (D) Muscle
(E) Skin
4. The answer is D [VIII B 2 a]. The patient's arterial PCO2 is lower than the normal
value of 40 mm Hg because hypoxemia has stimulated peripheral
chemoreceptors to increase his breathing rate; hyperventilation causes the
patient to blow off extra CO2 and results in respiratory alkalosis. In an obstructive
disease, such as asthma, both forced expiratory volume (FEV1) and forced vital
capacity (FVC) are decreased, with the larger decrease occurring in FEV1.
Therefore, the FEV1/FVC ratio is decreased. Poor ventilation of the affected areas
decreases the V/Q ratio and causes hypoxemia. The patient's residual volume
(RV) is increased because he is breathing at a higher lung volume to offset the
increased resistance of his airways.
4. Which of the following statements about this patient is most likely to be true?
(A) Forced expiratory volume/forced vital capacity (FEV1/FVC) is increased
(B) Ventilation/perfusion (V/Q) ratio is increased in the affected areas of his lungs
(C) His arterial PCO2 is higher than normal because of inadequate gas exchange
(D) His arterial PCO2 is lower than normal because hypoxemia is causing him to
hyperventilate
(E) His residual volume (RV) is decreased
5. The answer is C [II E 3 a (2)]. A cause of airway obstruction in asthma is
bronchiolar constriction. β2-adrenergic stimulation (β2-adrenergic agonists)
produces relaxation of the bronchioles.