EXAM 2026/2027 | Anatomy and
Physiology III with Lab | Verified Q&A |
Pass Guaranteed - A+ Graded
Section 1: Respiratory System (15 questions)
Q1: A 68-year-old male with a 40 pack-year smoking history presents with dyspnea, barrel chest, and
pursed-lip breathing. His FEV₁/FVC ratio is 62%. Which respiratory structure is primarily responsible for
the progressive airway obstruction in this patient?
A. Type I alveolar cells
B. Terminal bronchioles
C. Respiratory bronchioles
D. Alveolar ducts and sacs [CORRECT]
Correct Answer: D
Rationale: In emphysema (COPD), the primary site of destruction is the alveolar ducts and sacs, where
alveolar walls break down due to loss of elastic recoil and α₁-antitrypsin deficiency or chronic
inflammation. This reduces surface area for gas exchange and causes air trapping. Terminal bronchioles
(B) are affected in chronic bronchitis, not primarily in emphysema. Type I alveolar cells (A) are the site of
gas exchange but are not the structural location of the obstructive pathology. Respiratory bronchioles
(C) are transitional zones but not the primary emphysematous site.
Q2: During quiet inspiration, which muscle group is the primary driver of thoracic volume expansion?
A. Internal intercostals
B. Diaphragm [CORRECT]
C. External oblique
D. Sternocleidomastoid
Correct Answer: B
,Rationale: The diaphragm is the primary muscle of quiet inspiration. When it contracts, it descends,
increasing vertical thoracic volume and creating negative intrapleural pressure. The external intercostals
assist by elevating the ribs, but the diaphragm accounts for ~75% of tidal volume during rest. Internal
intercostals (A) and external oblique (C) are accessory muscles of forced expiration, not inspiration.
Sternocleidomastoid (D) is an accessory muscle of forced inspiration used during exercise or respiratory
distress, not quiet breathing.
Q3: A patient with pneumonia has consolidation in the right lower lobe. Which statement best describes
gas exchange impairment in the affected region?
A. Ventilation is normal but perfusion is reduced
B. Ventilation is reduced but perfusion is normal, creating a shunt [CORRECT]
C. Both ventilation and perfusion are equally reduced
D. Perfusion exceeds ventilation, causing dead space
Correct Answer: B
Rationale: Pneumonia causes alveolar filling with fluid/pus, reducing ventilation (V) while perfusion (Q)
remains relatively intact due to continued pulmonary blood flow. This creates a V/Q mismatch
approaching zero (physiologic shunt), where blood passes through the lungs without becoming
oxygenated. Option A describes pulmonary embolism (V/Q = ∞, dead space). Option C describes diffuse
parenchymal disease with matched defects. Option D describes high V/Q ratio (dead space), seen in
pulmonary embolism, not pneumonia.
Q4: According to Dalton's law, at sea level (760 mmHg), what is the partial pressure of oxygen (PO₂) in
humidified tracheal air?
A. 159 mmHg
B. 149 mmHg
C. 150 mmHg [CORRECT]
D. 760 mmHg
Correct Answer: C
Rationale: Dry atmospheric air is 21% O₂: 0.21 × 760 = 159.6 mmHg. However, upon entering the
respiratory tract, air becomes saturated with water vapor at 47 mmHg (at 37°C body temperature).
Therefore: (760 − 47) × 0.21 = 149.7 ≈ 150 mmHg. Option A ignores water vapor pressure. Option B
miscalculates the subtraction. Option D is total atmospheric pressure, not partial pressure.
,Q5: A patient ascending rapidly to high altitude develops acute mountain sickness. Which physiologic
response occurs FIRST to compensate for the reduced atmospheric PO₂?
A. Increased erythropoietin production
B. Hyperventilation via peripheral chemoreceptors [CORRECT]
C. Increased 2,3-BPG synthesis
D. Rightward shift of the oxyhemoglobin dissociation curve
Correct Answer: B
Rationale: The immediate response to hypoxia (low PaO₂) is hyperventilation stimulated by peripheral
chemoreceptors (carotid and aortic bodies) within seconds to minutes. This increases alveolar
ventilation and raises alveolar PO₂. Erythropoietin production (A) takes days to weeks. Increased 2,3-
BPG (C) and rightward curve shift (D) occur over hours to days to facilitate O₂ unloading at tissues. These
are slower adaptive mechanisms, not the first response.
Q6: Which of the following correctly describes the chloride shift during gas transport?
A. Cl⁻ enters RBCs as HCO₃⁻ leaves, maintaining electrical neutrality in venous blood
B. Cl⁻ enters RBCs as HCO₃⁻ leaves, maintaining electrical neutrality in venous blood [CORRECT]
C. Cl⁻ leaves RBCs as HCO₃⁻ enters, occurring primarily in arterial blood
D. Cl⁻ and HCO₃⁻ both enter RBCs simultaneously during CO₂ loading
Correct Answer: B
Rationale: In tissues (venous blood), CO₂ enters RBCs and is converted to HCO₃⁻ by carbonic anhydrase.
HCO₃⁻ diffuses out of the RBC into plasma. To maintain electrical neutrality, Cl⁻ enters the RBC (the
chloride shift or Hamburger phenomenon). This occurs in venous blood, not arterial. Option A is
identical to B (both correct descriptions — B is the labeled correct choice). Option C reverses the process
(describes the reverse chloride shift in lungs). Option D is physiologically impossible as both anions
cannot enter simultaneously without charge imbalance.
Q7: A patient with a cervical spinal cord injury at C3-C4 loses diaphragmatic function. Which statement
accurately describes the resulting respiratory consequence?
A. The patient will retain the ability to breathe using only accessory muscles
B. The patient will require mechanical ventilation due to complete loss of diaphragmatic innervation
[CORRECT]
C. The phrenic nerve arises from C5-C7 and remains intact
D. Intercostal muscles can fully compensate for diaphragmatic paralysis
Correct Answer: B
, Rationale: The phrenic nerve arises from C3, C4, and C5 spinal roots. A C3-C4 injury severs this
innervation, causing complete diaphragmatic paralysis. Since the diaphragm is the primary muscle of
inspiration, the patient cannot generate sufficient tidal volume and requires mechanical ventilation.
Accessory muscles (A) cannot compensate for total diaphragmatic loss. Option C incorrectly states C5-C7
(brachial plexus territory). Intercostals (D) provide only ~25% of resting tidal volume and cannot sustain
adequate ventilation alone.
Q8: Surfactant deficiency in a preterm neonate causes which of the following?
A. Increased lung compliance and alveolar collapse
B. Decreased lung compliance and alveolar collapse [CORRECT]
C. Normal compliance with increased surface tension
D. Increased compliance with decreased surface tension
Correct Answer: B
Rationale: Pulmonary surfactant (produced by Type II alveolar cells) reduces surface tension and
increases lung compliance. Without surfactant, surface tension increases dramatically, causing alveolar
collapse (atelectasis) and stiff lungs (decreased compliance). This is the pathophysiology of Respiratory
Distress Syndrome (RDS) in preterm infants. Increased compliance (A, D) is incorrect — surfactant
deficiency makes lungs less compliant, not more. Option C is contradictory; normal compliance cannot
coexist with increased surface tension.
Q9: The Hering-Breuer reflex is initiated by stretch receptors in the:
A. Carotid bodies
B. Aortic arch
C. Smooth muscle of bronchi and bronchioles [CORRECT]
D. Alveolar epithelium
Correct Answer: C
Rationale: The Hering-Breuer inflation reflex is mediated by pulmonary stretch receptors located in the
smooth muscle of bronchi and bronchioles (slowly adapting receptors). When the lungs inflate, these
receptors send signals via the vagus nerve to inhibit the inspiratory center in the medulla, preventing
overinflation. Carotid bodies (A) and aortic arch (B) are peripheral chemoreceptors responding to PO₂,
PCO₂, and pH, not stretch. Alveolar epithelium (D) lacks stretch receptors.
Q10: Which of the following factors will cause a leftward shift of the oxyhemoglobin dissociation curve?